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Atg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia

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dc.contributor.author이명식-
dc.date.accessioned2019-07-11T03:16:31Z-
dc.date.available2019-07-11T03:16:31Z-
dc.date.issued2019-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/169898-
dc.description.abstractProlonged 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 (Atg7Δpc) mice. In hypokalemic Atg7-floxed (Atg7f/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 Atg7Δpc 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 Atg7f/f and Atg7Δpc 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.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherNature Publishing Group-
dc.relation.isPartOfSCIENTIFIC REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleAtg7-dependent canonical autophagy regulates the degradation of aquaporin 2 in prolonged hypokalemia-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentBioMedical Science Institute (의생명과학부)-
dc.contributor.googleauthorWan-Young Kim-
dc.contributor.googleauthorSun Ah Nam-
dc.contributor.googleauthorArum Choi-
dc.contributor.googleauthorYu-Mi Kim-
dc.contributor.googleauthorSang Hee Park-
dc.contributor.googleauthorHong Lim Kim-
dc.contributor.googleauthorHyang Kim-
dc.contributor.googleauthorKi-Hwan Han-
dc.contributor.googleauthorChul Woo Yang-
dc.contributor.googleauthorMyung-Shik Lee-
dc.contributor.googleauthorYong Kyun Kim-
dc.contributor.googleauthorJin Kim-
dc.identifier.doi10.1038/s41598-019-39702-4-
dc.contributor.localIdA02752-
dc.relation.journalcodeJ02646-
dc.identifier.eissn2045-2322-
dc.identifier.pmid30816234-
dc.contributor.alternativeNameLee, Myung Shik-
dc.contributor.affiliatedAuthor이명식-
dc.citation.volume9-
dc.citation.number1-
dc.citation.startPage3021-
dc.identifier.bibliographicCitationSCIENTIFIC REPORTS, Vol.9(1) : 3021, 2019-
dc.identifier.rimsid62606-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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