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All-Trans Retinoic Acid Has a Potential Therapeutic Role for Diabetic Nephropathy

DC FieldValueLanguage
dc.contributor.author안철우-
dc.contributor.author김경래-
dc.contributor.author박종숙-
dc.date.accessioned2016-02-04T11:55:32Z-
dc.date.available2016-02-04T11:55:32Z-
dc.date.issued2015-
dc.identifier.issn0513-5796-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/141503-
dc.description.abstractPURPOSE: The aim of this study was to examine the effects of all-trans retinoic acid (ATRA) on diabetic nephropathy. MATERIALS AND METHODS: We measured amounts of urinary albumin excretion (UAE) after administrating ATRA to Otsuka Long-Evans Tokushima Fatty (OLETF) rats. In order to understand the mechanism of action for ATRA, we administrated ATRA to examine its inhibitory action on the production of transforming growth factor-β₁ (TGF-β₁), protein kinase C (PKC), and reactive oxidative stress (ROS) in cultured rat mesangial cells (RMCs). RESULTS: After 16 weeks of treatment, UAE was lower in the ATRA-treated OLETF rats than in the non-treated OLETF rats (0.07±0.03 mg/mgCr vs. 0.17±0.15 mg/mgCr, p<0.01). After incubation of RMCs in media containing 30 or 5 mM of glucose, treatment with ATRA showed time- and dose-dependent decreases in TGF-β₁ levels and ROS. Moreover, ATRA treatment showed a dose-dependent decrease in PKC expression. CONCLUSION: ATRA treatment suppressed UAE and TGF-β₁ synthesis, which was mediated by significant reductions in PKC activity and ROS production. Our results suggest that ATRA has a potential therapeutic role for diabetic nephropathy.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1597~1603-
dc.relation.isPartOfYonsei Medical Journal-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleAll-Trans Retinoic Acid Has a Potential Therapeutic Role for Diabetic Nephropathy-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorChul Sik Kim-
dc.contributor.googleauthorJong Suk Park-
dc.contributor.googleauthorChul Woo Ahn-
dc.contributor.googleauthorKyung Rae Kim-
dc.identifier.doi10.3349/ymj.2015.56.6.1597-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02270-
dc.contributor.localIdA00294-
dc.contributor.localIdA01660-
dc.relation.journalcodeJ02813-
dc.contributor.alternativeNameAhn, Chul Woo-
dc.contributor.alternativeNameKim, Kyung Rae-
dc.contributor.alternativeNamePark, Jong Suk-
dc.contributor.affiliatedAuthorAhn, Chul Woo-
dc.contributor.affiliatedAuthorKim, Kyung Rae-
dc.contributor.affiliatedAuthorPark, Jong Suk-
dc.rights.accessRightsfree-
dc.citation.volume56-
dc.citation.number6-
dc.citation.startPage1597-
dc.citation.endPage1603-
dc.identifier.bibliographicCitationYonsei Medical Journal, Vol.56(6) : 1597-1603, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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