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dc.contributor.author김승정-
dc.contributor.author류정화-
dc.date.accessioned2019-12-03T16:30:13Z-
dc.date.available2019-12-03T16:30:13Z-
dc.date.issued2019-
dc.identifier.issn1018-1172-
dc.identifier.issn1423-0135-
dc.identifier.otherOAK-26086-
dc.identifier.urihttp://dspace.ewha.ac.kr/handle/2015.oak/252258-
dc.description.abstractVascular access stenosis predominantly occurs as a result of neointimal hyperplasia (NH) formation at the anastomosis. Moreover, in the presence of NH, transforming growth factor-beta (TGF-beta) promotes vascular smooth muscle cell (VSMC) proliferation. Extracellular vesicles (EVs) released by endothelial cells are closely associated with vascular dysfunction. Here, we investigated the effects of EVs on TGF-beta signaling and VSMC proliferation. Specifically, EVs were collected from the culture medium of indoxyl sulfate (IS)-treated human umbilical vein endothelial cells and used (2 x 10(6)) to stimulate human aortic smooth muscle cells (SMCs) (1 x 10(6)). Western blotting was performed to assess the levels of Akt, ERK1/2, p38 MAPK, and Smad3. BrdU proliferation assays, quantitative PCR, and ELISA assays were performed to evaluate SMC proliferation and TGF-beta production. The IS-induced EVs stimulated the proliferation of aortic SMCs in a concentration-dependent manner. The EVs both contained TGF-beta and promoted TGF-beta production by SMCs by phosphorylating Akt, ERK1/2, p38 MAPK, and Smad3, which was significantly inhibited by an anti-TGF-beta antibody. SMC proliferation was suppressed by both an anti-TGF-beta antibody and inhibitors of the downstream factors. These results suggest that EVs are involved in the pathogenesis of vascular access stenosis by modulating TGF-beta signaling in VSMCs under uremic conditions.-
dc.languageEnglish-
dc.publisherKARGER-
dc.subjectNeointimal hyperplasia-
dc.subjectExtracellular vesicles-
dc.subjectEndothelium-
dc.subjectTransforming growth factor-beta-
dc.subjectVascular smooth muscle cells-
dc.titleIndoxyl Sulfate-Induced Extracellular Vesicles Released from Endothelial Cells Stimulate Vascular Smooth Muscle Cell Proliferation by Inducing Transforming Growth Factor-Beta Production-
dc.typeArticle-
dc.relation.issue3-
dc.relation.volume56-
dc.relation.indexSCIE-
dc.relation.indexSCOPUS-
dc.relation.startpage129-
dc.relation.lastpage138-
dc.relation.journaltitleJOURNAL OF VASCULAR RESEARCH-
dc.identifier.doi10.1159/000496796-
dc.identifier.wosidWOS:000496485200003-
dc.author.googleRyu, Jung-Hwa-
dc.author.googleJeon, Eun-Young-
dc.author.googleKim, Seung-Jung-
dc.contributor.scopusid김승정(8619054500)-
dc.date.modifydate20200517081002-
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의과대학 > 의학과 > Journal papers
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