{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,31]],"date-time":"2026-01-31T04:41:24Z","timestamp":1769834484477,"version":"3.49.0"},"reference-count":38,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,1,9]],"date-time":"2012-01-09T00:00:00Z","timestamp":1326067200000},"content-version":"vor","delay-in-days":2291,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biology of the Cell"],"published-print":{"date-parts":[[2005,10]]},"abstract":"<jats:p><jats:italic>Background information<\/jats:italic>. Phenotype analysis has demonstrated that AQP3 (aquaporin 3) null mice are polyuric and manifest a urinary concentration defect. In the present study, we report that deletion of AQP3 is also associated with an increased urinary sodium excretion. To investigate further the mechanism of the decreased urinary concentration and significant natriuresis, we examined the segmental and subcellular localization of collecting duct AQPs [AQP2, p\u2010AQP2 (phosphorylated AQP2), AQP3 and AQP4], ENaC (epithelial sodium channel) subunits and Na, K\u2010ATPase by immunoperoxidase and immunofluorescence microscopy in AQP3 null (\u2212\/\u2212), heterozygous (+\/\u2212) mice, wild\u2010type and unrelated strain of normal mice.<\/jats:p><jats:p><jats:italic>Results<\/jats:italic>. The present study confirms that AQP3 null mice exhibit severe polyuria and polydipsia and demonstrated that they exhibit increased urinary sodium excretion. In AQP3 null mice, there is a marked down\u2010regulation of AQP2 and p\u2010AQP2 both in CNT (connecting tubule) and CCD (cortical collecting duct). Moreover, AQP4 is virtually absent from CNT and CCD in AQP3 null mice. Basolateral AQP2 was virtually absent from AQP3 null mice and normal mice in contrast with rat. Thus the above results demonstrate that no basolateral AQPs are expressed in CNT and CCD of AQP3 null mice. However, in the medullary\u2010collecting ducts, there is no difference in the expression levels and subcellular localization of AQP2, p\u2010AQP2 and AQP4 between AQP3 +\/\u2212 and AQP3 null mice. Moreover, a striking decrease in the immunolabelling of the \u03b11 subunit of Na, K\u2010ATPase was observed in CCD in AQP3 null mice, whereas a medullary\u2010collecting duct exhibited normal labelling. Immunolabelling of all the ENaC subunits in the collecting duct was comparable between the two groups.<\/jats:p><jats:p><jats:italic>Conclusions<\/jats:italic>. The results improve the possibility that the severe urinary concentrating defect in AQP3 null mice may in part be caused by the decreased expression of AQP2, p\u2010AQP2 and AQP4 in CNT and CCD, whereas the increased urinary sodium excretion may in part be accounted for by Na, K\u2010ATPase in CCD in AQP3 null mice.<\/jats:p>","DOI":"10.1042\/bc20040148","type":"journal-article","created":{"date-parts":[[2005,9,26]],"date-time":"2005-09-26T14:46:50Z","timestamp":1127746010000},"page":"765-778","source":"Crossref","is-referenced-by-count":32,"title":["Decreased expression of AQP2 and AQP4 water channels and Na, K\u2010ATPase in kidney collecting duct in AQP3 null mice"],"prefix":"10.1111","volume":"97","author":[{"given":"Soo","family":"Wan Kim","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Veronika","family":"Gresz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aleksandra","family":"Rojek","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"A.S.","family":"Verkman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2012,1,9]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"crossref","first-page":"764","DOI":"10.1681\/ASN.V114764","article-title":"Homer W. 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