Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 한기환 | * |
dc.date.accessioned | 2019-03-27T16:30:06Z | - |
dc.date.available | 2019-03-27T16:30:06Z | - |
dc.date.issued | 2019 | * |
dc.identifier.issn | 2045-2322 | * |
dc.identifier.other | OAK-24506 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/249511 | - |
dc.description.abstract | Prolonged hypokalemia induces a decrease of urinary concentrating ability via down-regulation of aquaporin 2 (AQP2); however, the precise mechanisms remain unknown. To investigate the role of autophagy in the degradation of AQP2, we generated the principal cell-specific Atg7 deletion (Atg7 Δpc ) mice. In hypokalemic Atg7-floxed (Atg7 f/f ) mice, huge irregular shaped LC3-positive autophagic vacuoles accumulated mainly in inner medullary collecting duct (IMCD) cells. Total- and pS261-AQP2 were redistributed from apical and subapical domains into these vacuoles, which were not co-localized with RAB9. However, in the IMCD cells of hypokalemic Atg7 Δpc mice, these canonical autophagic vacuoles were markedly reduced, whereas numerous small regular shaped LC3-negative/RAB9-positive non-canonical autophagic vacuoles were observed along with diffusely distributed total- and pS261-AQP2 in the cytoplasm. The immunoreactivity of pS256-AQP2 in the apical membrane of IMCD cells was markedly decreased, and no redistribution was observed in both hypokalemic Atg7 f/f and Atg7 Δpc mice. These findings suggest that AQP2 down regulation in hypokalemia was induced by reduced phosphorylation of AQP2, resulting in a reduction of apical plasma labeling of pS256-AQP2 and degradation of total- and pS261-AQP2 via an LC3/ATG7-dependent canonical autophagy pathway. © 2019, The Author(s). | * |
dc.language | English | * |
dc.publisher | Nature Publishing Group | * |
dc.title | Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia | * |
dc.type | Article | * |
dc.relation.issue | 1 | * |
dc.relation.volume | 9 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.journaltitle | Scientific Reports | * |
dc.identifier.doi | 10.1038/s41598-019-39702-4 | * |
dc.identifier.wosid | WOS:000459891700031 | * |
dc.identifier.scopusid | 2-s2.0-85062275853 | * |
dc.author.google | Kim W.-Y. | * |
dc.author.google | Nam S.A. | * |
dc.author.google | Choi A. | * |
dc.author.google | Kim Y.-M. | * |
dc.author.google | Park S.H. | * |
dc.author.google | Kim H.L. | * |
dc.author.google | Kim H. | * |
dc.author.google | Han K.-H. | * |
dc.author.google | Yang C.W. | * |
dc.author.google | Lee M.-S. | * |
dc.author.google | Kim Y.K. | * |
dc.author.google | Kim J. | * |
dc.contributor.scopusid | 한기환(14622504200) | * |
dc.date.modifydate | 20240123095704 | * |