Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 하헌주 | * |
dc.date.accessioned | 2016-08-28T12:08:37Z | - |
dc.date.available | 2016-08-28T12:08:37Z | - |
dc.date.issued | 2009 | * |
dc.identifier.issn | 0250-8095 | * |
dc.identifier.other | OAK-6142 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/220416 | - |
dc.description.abstract | Background/Aims: Plasminogen activator inhibitor (PAI)-1 is increasingly recognized as a profibrotic factor but the mechanisms are not entirely clear. The present study examined the profibrotic mechanism of PAI-1 focusing on its effect on transforming growth factor (TGF)-β1 in experimental diabetes. Methods: PAI-1 knockout (KO) mesangial cells cultured under high glucose (HG) in addition to streptozotocin-induced diabetic PAI-1 KO mice were used. Results: PAI-1 deficiency did not affect plasma glucose significantly but reduced the fractional mesangial area, fibronectin and collagen I expression in the renal cortex after 20 weeks of diabetes as well as in HG-stimulated mesangial cells along with suppression of TGF-β1 mRNA expression. PAI-1 deficiency also reduced HG-induced βig-h3, a TGF-β1-induced gene product, mRNA expression. All these losses-of-function in PAI-1 KO mesangial cells were effectively gained by recombinant PAI-1. Recombinant PAI-1-induced fibronectin and collagen I expression was abrogated by TGF-β1 receptor inhibitor or anti-TGF-β antibody suggesting that the effect of PAI-1 was mediated by TGF-β1. In a similar context, recombinant PAI-1 stimulated TGF-β1 promoter activity to the same extent as TGF-β1 itself. Conclusion: Since TGF-β1 is well known to stimulate the PAI-1 promoter, we suggest that TGF-β1 and PAI-1 together constitute a positive feedback loop in the development of renal fibrosis in diabetes. Copyright © 2009 S. Karger AG, Basel. | * |
dc.language | English | * |
dc.title | Positive feedback loop between plasminogen activator inhibitor-1 and transforming growth factor-beta1 during renal fibrosis in diabetes | * |
dc.type | Article | * |
dc.relation.issue | 6 | * |
dc.relation.volume | 30 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 481 | * |
dc.relation.lastpage | 490 | * |
dc.relation.journaltitle | American Journal of Nephrology | * |
dc.identifier.doi | 10.1159/000242477 | * |
dc.identifier.wosid | WOS:000272892800001 | * |
dc.identifier.scopusid | 2-s2.0-70349409438 | * |
dc.author.google | Seo J.Y. | * |
dc.author.google | Park J. | * |
dc.author.google | Yu M.R. | * |
dc.author.google | Kim Y.S. | * |
dc.author.google | Ha H. | * |
dc.author.google | Lee H.B. | * |
dc.contributor.scopusid | 하헌주(7202277106) | * |
dc.date.modifydate | 20240422113229 | * |