IR@PKUHSC  > 北京大学基础医学院  > 心血管所
学科主题基础医学
Rosiglitazone inhibits angiotensin II-induced CTGF expression in vascular smooth muscle cells - Role of PPAR-gamma in vascular fibrosis
Gao, Deng-Feng; Niu, Xiao-Lin; Hao, Guang-Hua; Peng, Ning; Wei, Jin; Ning, Ning; Wang, Nan-Ping
关键词angiotensin connective tissue growth factor hypertension PPAR-gamma smooth muscle
刊名BIOCHEMICAL PHARMACOLOGY
2007-01-15
DOI10.1016/j.bcp.2006.09.019
73期:2页:185-197
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy
研究领域[WOS]Pharmacology & Pharmacy
关键词[WOS]ACTIVATED-RECEPTOR-GAMMA ; TISSUE GROWTH-FACTOR ; SPONTANEOUSLY HYPERTENSIVE-RATS ; FACTOR-BETA ; EXTRACELLULAR-MATRIX ; ENDOTHELIAL FUNCTION ; CARDIAC FIBROBLASTS ; TYPE-1 RECEPTOR ; MESANGIAL CELLS ; BLOOD-VESSELS
英文摘要

Angiotensin (Ang) II plays a pivotal role in vascular fibrosis, which leads to serious complications in hypertension and diabetes. Connective tissue growth factor (CTGF) is a potent profibrotic factor implicated in the Ang II-induced pathologic fibrosis process. PPAR-gamma activators thiazolidinediones have been recently reported to have beneficial vascular effects. However, their effects and related molecular mechanisms on extracellular matrix (ECM) turnover in vascular smooth muscle Cells (VSMCs) are unknown. The present study evaluated the regulation of Ang II-induced CTGF, ECM production and cell growth by rosiglitazone in VSMCs. In aorta of Ang II-infused rats, CTGF expression was markedly increased, and type III Collagen and fibronectin overexpression was observed. Cotreatment with rosiglitazone diminished these changes, whereas increased nuclear PPAR-gamma expression in VSMCs. In growth-arrested VSMCs, rosiglitazone attenuated the proliferation and apoptosis, increased PPAR-gamma production and activation, and reduced CTGF and ECM production in response to Ang II in a dose-dependent fashion. These inhibitory effects were attenuated by the pretreatment of cells with PPAR-gamma antagonist GW9662 or bisphenol A diglycidyl ether (BADGE). Furthermore, rosiglitazone inhibited Ang II-induced Smad2 production and phosphorylation but had no effect on transforming growth factor-beta(1) (TGF-B-1) expression. These results suggest that in Ang II-stimulated VSMCs, rosiglitazone caused an antiproliferative, antiapototic effect and reduces ECM production through mechanisms that include reducing CTGF expression, and a crosstalk between PPAR-gamma and Smad may be involved in the inhibitory effects of rosiglitazone. This novel finding suggests a role of PPAR-gamma activators in preventing Ang II-induced vascular fibrosis. (c) 2006 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000243616100003
引用统计
被引频次:38[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61058
专题北京大学基础医学院_心血管所
作者单位1.Xian Jiaotong Univ, Sch Med, Affiliated Hosp 2, Dept Cardiol, Xian 710004, Shaanxi, Peoples R China
2.Xian Jiaotong Univ, Minist Educ, Key Lab Environm & Genes Related Dis, Xian 710061, Peoples R China
3.Xian Jiaotong Univ, Dept Pharmacol, Xian 710061, Shaanxi, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Inst Cardiovasc Sci, Beijing 100083, Peoples R China
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Gao, Deng-Feng,Niu, Xiao-Lin,Hao, Guang-Hua,et al. Rosiglitazone inhibits angiotensin II-induced CTGF expression in vascular smooth muscle cells - Role of PPAR-gamma in vascular fibrosis[J]. BIOCHEMICAL PHARMACOLOGY,2007,73(2):185-197.
APA Gao, Deng-Feng.,Niu, Xiao-Lin.,Hao, Guang-Hua.,Peng, Ning.,Wei, Jin.,...&Wang, Nan-Ping.(2007).Rosiglitazone inhibits angiotensin II-induced CTGF expression in vascular smooth muscle cells - Role of PPAR-gamma in vascular fibrosis.BIOCHEMICAL PHARMACOLOGY,73(2),185-197.
MLA Gao, Deng-Feng,et al."Rosiglitazone inhibits angiotensin II-induced CTGF expression in vascular smooth muscle cells - Role of PPAR-gamma in vascular fibrosis".BIOCHEMICAL PHARMACOLOGY 73.2(2007):185-197.
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