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Colchicine Ameliorates High Glucose-Induced ICAM-1 and Fibronectin Expression in Renal Cells via Inhibiting Locally-Produced Angiotensin II.

DC Field Value Language
dc.contributor.author강신욱-
dc.contributor.author김은진-
dc.contributor.author박정탁-
dc.contributor.author박희진-
dc.contributor.author석한나-
dc.contributor.author유태현-
dc.contributor.author이용강-
dc.contributor.author한승혁-
dc.date.accessioned2014-12-20T17:30:42Z-
dc.date.available2014-12-20T17:30:42Z-
dc.date.issued2011-
dc.identifier.issn1975-9460-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/94735-
dc.description.abstractPURPOSE: A previous study has demonstrated that colchicine abrogated intercellular adhesion molecule (ICAM)-1 and fibronectin expression in renal cells exposed to high glucose media, but the underlying mechanism was not clarified. This study was undertaken to elucidate whether it was attributed to the inhibitory effect of colchicine on locally-produced angiotensin II (AII) under diabetic conditions. METHODS: Rat mesangial cells and NRK-52E cells were cultured in media containing 5.6 mM glucose (NG), NG+10(-7) M AII (NG+AII), or 30 mM glucose (HG) with or without 10(-8) M colchicine (Col) and/or 10(-6) M L-158,809, an AII type 1 receptor blocker (ARB). ICAM-1 and fibronectin mRNA and protein expressions were determined by real-time PCR (RT-PCR) and Western blot, respectively. AII levels in conditioned media were determined by ELISA. RESULTS: AII levels in conditioned media were significantly higher in HG-stimulated mesangial cells and NRK-52E cells compared to NG cells (p<0.05). ICAM-1 and fibronectin mRNA and protein expression were significantly increased in renal cells exposed to HG media (p<0.05 or p<0.01), and these increases were significantly ameliorated by colchicine or ARB treatment (p<0.05). Colchicine and ARB also significantly attenuated AII-induced ICAM-1 and fibronectin expression (p<0.05). However, there was no additive inhibitory effect of colchicine and ARB on the increases in ICAM-1 and fibronectin expression. CONCLUSION: Colchicine abrogated increased ICAM-1 and fibronectin expression in renal cells under diabetic conditions, which is partly mediated by inhibiting HG-induced locally-produced AII. These findings provide a new renoprotective mechanism of colchicine in diabetic nephropathy in addition to its impact on leukocyte functions-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfKorean Journal of Nephrology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleColchicine Ameliorates High Glucose-Induced ICAM-1 and Fibronectin Expression in Renal Cells via Inhibiting Locally-Produced Angiotensin II.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorEun Jin Kim-
dc.contributor.googleauthorDong Ho Shin-
dc.contributor.googleauthorJin Ji Li-
dc.contributor.googleauthorSun Ha Lee-
dc.contributor.googleauthorYong Kang Lee-
dc.contributor.googleauthorHee-Jin Park-
dc.contributor.googleauthorHannah Seok-
dc.contributor.googleauthorJung Tak Park-
dc.contributor.googleauthorSeung Hyeok Han-
dc.contributor.googleauthorTae-Hyun Yoo-
dc.contributor.googleauthorShin-Wook Kang-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00053-
dc.contributor.localIdA01654-
dc.contributor.localIdA01778-
dc.contributor.localIdA01930-
dc.contributor.localIdA02097-
dc.contributor.localIdA02526-
dc.contributor.localIdA02973-
dc.contributor.localIdA04304-
dc.contributor.localIdA00823-
dc.relation.journalcodeJ02065-
dc.subject.keywordColchicine-
dc.subject.keywordDiabetic nephropathy-
dc.subject.keywordRenin-angiotensin system-
dc.subject.keywordICAM-1-
dc.subject.keywordFibronectin-
dc.contributor.alternativeNameKang, Shin Wook-
dc.contributor.alternativeNameKim, Eun Jin-
dc.contributor.alternativeNamePark, Jung Tak-
dc.contributor.alternativeNamePark, Hee Jin-
dc.contributor.alternativeNameSeok, Hannah-
dc.contributor.alternativeNameShin, Dong Ho-
dc.contributor.alternativeNameYoo, Tae Hyun-
dc.contributor.alternativeNameLee, Yong Kang-
dc.contributor.alternativeNameHan, Seung Hyeok-
dc.contributor.affiliatedAuthorKang, Shin Wook-
dc.contributor.affiliatedAuthorPark, Jung Tak-
dc.contributor.affiliatedAuthorPark, Hee Jin-
dc.contributor.affiliatedAuthorSeok, Hannah-
dc.contributor.affiliatedAuthorShin, Dong Ho-
dc.contributor.affiliatedAuthorYoo, Tae Hyun-
dc.contributor.affiliatedAuthorLee, Yong Kang-
dc.contributor.affiliatedAuthorHan, Seung Hyeok-
dc.contributor.affiliatedAuthorKim, Eun Jin-
dc.rights.accessRightsfree-
dc.citation.volume30-
dc.citation.number6-
dc.citation.startPage575-
dc.citation.endPage584-
dc.identifier.bibliographicCitationKorean Journal of Nephrology, Vol.30(6) : 575-584, 2011-
dc.identifier.rimsid27720-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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