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Anti-proliferative effect of rosiglitazone on angiotensin II-induced vascular smooth muscle cell proliferation is mediated by the mTOR pathway

DC Field Value Language
dc.contributor.author차민지-
dc.contributor.author최은미-
dc.contributor.author김일권-
dc.contributor.author함온주-
dc.contributor.author김중선-
dc.contributor.author황기철-
dc.contributor.author송병욱-
dc.contributor.author이세연-
dc.contributor.author임소연-
dc.contributor.author장양수-
dc.date.accessioned2014-12-19T16:38:10Z-
dc.date.available2014-12-19T16:38:10Z-
dc.date.issued2012-
dc.identifier.issn1065-6995-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/89902-
dc.description.abstractVSMC (vascular smooth muscle cell) proliferation contributes significantly to intimal thickening in atherosclerosis, restenosis and venous bypass graft diseases. Ang II (angiotensin II) has been implicated in VSMC proliferation though the activation of multiple growth-promoting signals. Although TZDs (thiazolidinediones) can inhibit VSMC proliferation and reduce Ang II-induced fibrosis, the mechanism underlying the inhibition of VSMC proliferation and fibrosis needs elucidation. We have used primary cultured rat aortic VSMCs and specific antibodies to investigate the inhibitory mechanism of rosiglitazone on Ang II-induced VSMC proliferation. Rosiglitazone treatment significantly inhibited Ang II-induced rat aortic VSMC proliferation in a dose-dependent manner. Western blot analysis showed that rosiglitazone significantly lowered phosphorylated ERK1/2 (extracellular-signal-regulated kinase 1/2), Akt (also known as protein kinase B), mTOR (mammalian target of rapamycin), p70S6K (70 kDa S6 kinase) and 4EBP1 (eukaryotic initiation factor 4E-binding protein) levels in Ang II-treated VSMCs. In addition, PPAR-γ (peroxisome-proliferator-activated receptor γ) mRNA increased significantly and CTGF (connective tissue growth factor), Fn (fibronectin) and Col III (collagen III) levels decreased significantly. The results demonstrate that the rosiglitazone directly inhibits the pro-atherosclerotic effect of Ang II on rat aortic VSMCs. It also attenuates Ang II-induced ECM (extracellular matrix) molecules and CTGF production in rat aortic VSMCs, reducing fibrosis. Importantly, PPAR-γ activation mediates these effects, in part, through the mTOR-p70S6K and -4EBP1 system.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfCELL BIOLOGY INTERNATIONAL-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAngiotensin II/metabolism*-
dc.subject.MESHAnimals-
dc.subject.MESHCell Proliferation*/drug effects-
dc.subject.MESHMuscle, Smooth, Vascular/cytology*-
dc.subject.MESHMuscle, Smooth, Vascular/metabolism-
dc.subject.MESHRats-
dc.subject.MESHSignal Transduction/drug effects-
dc.subject.MESHTOR Serine-Threonine Kinases/metabolism*-
dc.subject.MESHThiazolidinediones/pharmacology*-
dc.titleAnti-proliferative effect of rosiglitazone on angiotensin II-induced vascular smooth muscle cell proliferation is mediated by the mTOR pathway-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorJung-Sun Kim-
dc.contributor.googleauthorIl-Kwon Kim-
dc.contributor.googleauthorSe-Yeon Lee-
dc.contributor.googleauthorByeong-Wook Song-
dc.contributor.googleauthorMin-Ji Cha-
dc.contributor.googleauthorHeesang Song-
dc.contributor.googleauthorEunmi Choi-
dc.contributor.googleauthorSoyeon Lim-
dc.contributor.googleauthorOnju Ham-
dc.contributor.googleauthorYangsoo Jang-
dc.contributor.googleauthorKi-Chul Hwang-
dc.identifier.doi22050182-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03995-
dc.contributor.localIdA04336-
dc.contributor.localIdA00961-
dc.contributor.localIdA04456-
dc.contributor.localIdA02026-
dc.contributor.localIdA02880-
dc.contributor.localIdA03448-
dc.contributor.localIdA04151-
dc.contributor.localIdA00848-
dc.contributor.localIdA03373-1-
dc.relation.journalcodeJ00477-
dc.identifier.eissn1095-8355-
dc.identifier.pmid22050182-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1042/CBI20100524/abstract-
dc.subject.keywordangiotensin II-
dc.subject.keywordmammalian target of rapamycin (mTOR)-
dc.subject.keywordproliferation-
dc.subject.keywordrosiglitazone-
dc.subject.keywordsmooth muscle cell-
dc.contributor.alternativeNameCha, Min Ji-
dc.contributor.alternativeNameChoi, Eun Mi-
dc.contributor.alternativeNameKim, Il Kwon-
dc.contributor.alternativeNameHam, On Ju-
dc.contributor.alternativeNameKim, Jung Sun-
dc.contributor.alternativeNameHwang, Ki Chul-
dc.contributor.alternativeNameSong, Byeong Wook-
dc.contributor.alternativeNameLee, Se Yeon-
dc.contributor.alternativeNameLim, So Yeon-
dc.contributor.alternativeNameJang, Yang Soo-
dc.contributor.affiliatedAuthorCha, Min Ji-
dc.contributor.affiliatedAuthorHam, On Ju-
dc.contributor.affiliatedAuthorKim, Jung Sun-
dc.contributor.affiliatedAuthorHwang, Ki Chul-
dc.contributor.affiliatedAuthorSong, Byeong Wook-
dc.contributor.affiliatedAuthorLee, Se Yeon-
dc.contributor.affiliatedAuthorJang, Yang Soo-
dc.contributor.affiliatedAuthorChoi, Eun Mi-
dc.contributor.affiliatedAuthorKim, Il Kwon-
dc.contributor.affiliatedAuthorLim, So Yeon-
dc.citation.volume36-
dc.citation.number3-
dc.citation.startPage305-
dc.citation.endPage310-
dc.identifier.bibliographicCitationCELL BIOLOGY INTERNATIONAL, Vol.36(3) : 305-310, 2012-
dc.identifier.rimsid31972-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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