Oncostatin M is expressed in atherosclerotic lesions: A role for Oncostatin M in the pathogenesis of atherosclerosis

被引：44

作者：

Albasanz-Puig, Adaia ^{[2
]}

Murray, Jacqueline ^{[2
]}

Preusch, Michael ^{[1
]}

Coan, Daniel ^{[2
]}

Namekata, Mayumi ^{[2
]}

Patel, Yatin ^{[3
]}

Dong, Zhao Ming ^{[1
,2
]}

Rosenfeld, Michael E. ^{[1
]}

Wijelath, Errol S. ^{[2
]}

机构：

[1] Univ Washington, Sch Med, Dept Pathol, Seattle, WA 98195 USA

[2] VA Puget Sound Hlth Care Syst, Dept Surg, Div Vasc Surg, Seattle, WA USA

[3] Kings Coll London, Sch Med London, Div Cardiovasc, Dept Cardiol, London, England

来源：

ATHEROSCLEROSIS | 2011年 / 216卷 / 02期

关键词：

Oncostatin M; Smooth muscle cell; Atherosclerosis; Carotid plaques; ApoE(-/-); STAT-1; STAT-3; SMOOTH-MUSCLE-CELLS; IN-VITRO; ENDOTHELIAL-CELLS; SIGNALING PATHWAY; CAROTID PLAQUE; ED-B; ANGIOGENESIS; INDUCTION; CYTOKINES; DISEASE;

D O I：

10.1016/j.atherosclerosis.2011.02.003

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Objective: Chronic inflammation plays a pivotal role in the development and progression of atherosclerosis. The inflammatory response is mediated by cytokines. The aim of this study was to determine if OncostatinM(OSM), a monocyte and T-lymphocyte specific cytokine is present in atherosclerotic lesions. We also investigated the roles of signal transducer and activator of transcription (STAT)-1 and STAT-3 in regulating OSM-induced smooth muscle cell (SMC) proliferation, migration and cellular fibronectin (cFN) synthesis. Methods and results: Immunostaining of atherosclerotic lesions from human carotid plaques demonstrated the expression of OSM antigen in both macrophages and SMCs. Explanted SMCs from human carotid plaques expressed OSM mRNA and protein as determined by RT-PCR and Western blotting. Using the chow-fed ApoE-/- mouse model of atherosclerosis, we observed that OSM was initially expressed in the intima at 20 weeks of age. By 30 weeks, OSM was expressed in both the intima and media. In vitro studies show that OSM promotes SMC proliferation, migration and cFN synthesis. Lentivirus mediated-inhibition of STAT-1 and STAT-3 prevented OSM-induced SMC proliferation, migration and cellular fibronectin synthesis. Conclusions: These findings demonstrate that OSM is expressed in atherosclerotic lesions and may contribute to the progression of atherosclerosis by promoting SMC proliferation, migration and extracellular matrix protein synthesis through the STAT pathway. Published by Elsevier Ireland Ltd.

引用

页码：292 / 298

页数：7

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