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学科主题临床医学
Agonists at PPAR-gamma suppress angiotensin II-induced production of plasminogen activator inhibitor-1 and extracellular matrix in rat cardiac fibroblasts
Hao, G-H1,2; Niu, X-L1,2; Gao, D-F1; Wei, J.1; Wang, N-P3
关键词PPAR-gamma angiotensin cardiac fibroblast plasminogen activator inhibitor-1 extracellular matrix rosiglitazone 15d-PGJ(2) fibrosis
刊名BRITISH JOURNAL OF PHARMACOLOGY
2008-04-01
DOI10.1038/bjp.2008.21
153期:7页:1409-1419
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]JUN NH2-TERMINAL KINASE ; RECEPTOR-GAMMA ; IN-VIVO ; VASCULAR FIBROSIS ; MYOCARDIAL-INFARCTION ; ENDOTHELIAL FUNCTION ; INCREASED EXPRESSION ; TYPE-1 EXPRESSION ; GENE-EXPRESSION ; STELLATE CELLS
英文摘要

Background and purpose: Peroxisome proliferator-activated receptor (PPAR)-gamma ligands have been shown to inhibit cardiac fibrosis. However, the underlying mechanisms are poorly understood. We investigated the regulation by PPAR-gamma ligands of angiotensin (Ang) II-induced plasminogen activator inhibitor (PAI)-1, extracellular matrix (ECM) production and cell growth in cardiac fibroblasts.

Experimental approach: The effects of PPAR-gamma ligands on Ang II-induced PAI-1, ECM expression and cell growth were assessed in primary-cultured rat cardiac fibroblasts; cardiac PAI-1 and ECM production was examined in Ang II-infused rats.

Key results: In growth-arrested cardiac fibroblasts, PPAR-gamma ligands rosiglitazone and 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) dose-dependently attenuated Ang II-induced cell proliferation and expression of PAI-1, collagen type-I, collagen type-III and fibronectin. An accompanying increase in PPAR-gamma expression and activation was also observed. These suppressive effects were attenuated by the PPAR-gamma antagonists GW9662 and bisphenol A diglycidyl ether ( BADGE). Moreover, rosiglitazone and 15d-PGJ(2) inhibited in part the expression and phosphorylation of Ang II-induced transforming growth factor ( TGF)-beta 1, Smad2/3 and c-Jun NH(2)-terminal kinase (JNK). Ang II infusion in rats markedly increased left ventricular production of PAI-1, collagen and fibronectin, with a concurrent increase in the ratios of heart weight/body weight and left ventricle weight/body weight. Co-treatment with rosiglitazone significantly decreased these levels and upregulated PPAR-gamma expression.

Conclusions and implications: Rosiglitazone and 15d-PGJ2 suppress Ang II-induced production of PAI-1 and ECM probably via interactions between PPAR-gamma and TGF-beta 1/Smad2/3 and JNK signalling pathways. It is suggested that PPAR-gamma and its ligands may have potential applications in preventing cardiac fibrosis.

语种英语
WOS记录号WOS:000254559700009
引用统计
被引频次:41[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/400002259/59349
专题北京大学第三临床医学院_心血管内科
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, Key Lab Environm & Genes Related Dis, Dept Cardiol, Minist Educ, Xian, Shaanxi, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Inst Cardiovasc Sci, Dept Cardiol, Beijing 100871, Peoples R China
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Hao, G-H,Niu, X-L,Gao, D-F,et al. Agonists at PPAR-gamma suppress angiotensin II-induced production of plasminogen activator inhibitor-1 and extracellular matrix in rat cardiac fibroblasts[J]. BRITISH JOURNAL OF PHARMACOLOGY,2008,153(7):1409-1419.
APA Hao, G-H,Niu, X-L,Gao, D-F,Wei, J.,&Wang, N-P.(2008).Agonists at PPAR-gamma suppress angiotensin II-induced production of plasminogen activator inhibitor-1 and extracellular matrix in rat cardiac fibroblasts.BRITISH JOURNAL OF PHARMACOLOGY,153(7),1409-1419.
MLA Hao, G-H,et al."Agonists at PPAR-gamma suppress angiotensin II-induced production of plasminogen activator inhibitor-1 and extracellular matrix in rat cardiac fibroblasts".BRITISH JOURNAL OF PHARMACOLOGY 153.7(2008):1409-1419.
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