Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 류동열 | * |
dc.date.accessioned | 2016-12-06T02:12:25Z | - |
dc.date.available | 2016-12-06T02:12:25Z | - |
dc.date.issued | 2008 | * |
dc.identifier.issn | 0363-6127 | * |
dc.identifier.other | OAK-5032 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/233017 | - |
dc.description.abstract | Monocyte chemoattractant protein-1 (MCP-1) is a potent chemokine that plays an important role in the recruitment of macrophages. Although previous studies have demonstrated the importance of MCP-1 in the pathogenesis of diabetic nephropathy (DN) in terms of inflammation, the role of MCP-1 and its receptor (C-C chemokine receptor 2; CCR2) in extracellular matrix (ECM) accumulation under diabetic conditions has been largely unexplored. This study was undertaken to investigate the functional role of the MCP-1/CCR2 system in high glucose-induced ECM (fibronectin and type IV collagen) protein expression in cultured mesangial cells (MCs). Mouse MCs were exposed to medium containing 5.6 mM glucose (NG), NG+24.4 mM mannitol (NG+M), or 30 mM glucose (HG) with or without mutant MCP-1 (mMCP-1), CCR2 small interfering (si)RNA, or CCR2 inhibitor (RS102895). To examine the relationship between MCP-1 and transforming growth factor (TGF)-β1, MCs were also treated with TGF-β1 (2 ng/ml) with or without mMCP-1 or CCR2 siRNA. Transient transfection was performed with Lipofectamine 2000 for 24 h. Cell viability was determined by an MTT assay, mouse and human MCP-1 and TGF-β1 levels by ELISA, and CCR2 and ECM protein expression by Western blotting. Transfections of mMCP-1 and CCR2 siRNA increased human MCP-1 levels and inhibited CCR2 expression, respectively. HG-induced ECM protein expression and TGF-β1 levels were significantly attenuated by mMCP-1, CCR2 siRNA, and RS102895 (P < 0.05). MCP-1 directly increased ECM protein expression, and this increase was inhibited by an anti-TGF-β1 antibody. In addition, TGF-β1-induced ECM protein expression was significantly abrogated by the inhibition of the MCP-1/CCR2 system (P < 0.05). These results suggest that an interaction between the MCP-1/CCR2 system and TGF-β1 may contribute to ECM accumulation in DN. Copyright © 2008 the American Physiological Society. | * |
dc.language | English | * |
dc.title | MCP-1/CCR2 system is involved in high glucose-induced fibronectin and type IV collagen expression in cultured mesangial cells | * |
dc.type | Article | * |
dc.relation.issue | 3 | * |
dc.relation.volume | 295 | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | F749 | * |
dc.relation.lastpage | F757 | * |
dc.relation.journaltitle | American Journal of Physiology - Renal Physiology | * |
dc.identifier.doi | 10.1152/ajprenal.00547.2007 | * |
dc.identifier.wosid | WOS:000258876800016 | * |
dc.identifier.scopusid | 2-s2.0-54449087814 | * |
dc.author.google | Park J. | * |
dc.author.google | Ryu D.-R. | * |
dc.author.google | Li J.J. | * |
dc.author.google | Jung D.-S. | * |
dc.author.google | Kwak S.-J. | * |
dc.author.google | Lee S.H. | * |
dc.author.google | Yoo T.-H. | * |
dc.author.google | Han S.H. | * |
dc.author.google | Lee J.E. | * |
dc.author.google | Kim D.K. | * |
dc.author.google | Moon S.J. | * |
dc.author.google | Kim K. | * |
dc.author.google | Han D.S. | * |
dc.author.google | Kang S.-W. | * |
dc.contributor.scopusid | 류동열(7103144218;56997547400;56669926200) | * |
dc.date.modifydate | 20240123102517 | * |