Asymmetric dimethylarginine confers the communication between endothelial and smooth muscle cells and leads to VSMC migration through p38 and ERK1/2 signaling cascade

被引：20

作者：

Sun, Lan ^{[1
,2
]}

Zhang, Tiantai ^{[1
,2
]}

Yu, Xin ^{[3
]}

Xin, Wenyu ^{[1
,2
]}

Lan, Xi ^{[1
,2
]}

Zhang, Dan ^{[1
,2
]}

Huang, Chao ^{[1
,2
]}

Du, Guahua ^{[1
,2
]}

机构：

[1] Chinese Acad Med Sci, Natl Ctr Pharmaceut Screening, Inst Mat Med, Beijing 100050, Peoples R China

[2] Peking Union Med Coll, Beijing 100050, Peoples R China

[3] Yantai Univ, Dept Geriatr Cardiol, Yantai, Peoples R China

来源：

FEBS LETTERS | 2011年 / 585卷 / 17期

基金：

美国国家科学基金会;

关键词：

Asymmetric dimethylarginine; Oxide LDL; Vascular smooth muscle cell; Atherosclerosis; Migration; MAPK; CHOLESTEROL-FED RABBITS; ENDOGENOUS INHIBITOR; INDUCED APOPTOSIS; EXPRESSION; PROLIFERATION; PATHWAY; PLASMA; KINASE;

D O I：

10.1016/j.febslet.2011.07.032

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Communication between endothelial and smooth muscle cells (SMCs) contributes to atherosclerosis induced by atherogenic factors, such as oxide LDL. Asymmetric dimethylarginine (ADMA), a newly found cardiovascular risk factor, accumulates in the culture medium of oxide LDL (oxLDL)-treated endothelial cells and positively correlates with atherosclerosis. This study demonstrates that ADMA mediates the communication between endothelial cells and SMCs induced by oxLDL leading to SMC migration. In addition, the present study suggests exogenous ADMA directly induces SMC migration via p38 and ERK1/2 MAPK signaling transduction way. Investigations to identify the factors regulating VSMC migration may provide novel insights into atherosclerosis and its complications. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：2727 / 2734

页数：8

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