ox-LDL induces endothelial dysfunction by promoting Arp2/3 complex expression

被引：20
|
作者：
Tang, Yao [1 ]
Zhao, Jianting [1 ]
Shen, Liming [1 ]
Jin, Yiqi [1 ]
Zhang, Zhixuan [1 ]
Xu, Guoxiong [1 ]
Huang, Xianchen [1 ]
机构：
[1] Nanjing Med Univ, Suzhou Hosp Affiliated, Suzhou Municipal Hosp, Vasc Surg, 26 Daoqian St, Suzhou 215002, Jiangsu, Peoples R China
来源：
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2016年 / 475卷 / 02期
关键词：
Arp2/3; ox-LDL; LOX-1; Rac-1; Endothelial dysfunction; LOW-DENSITY-LIPOPROTEIN; CELL-SHAPE; ACTIN; ATHEROSCLEROSIS; ATHEROGENESIS; ACTIVATION; GAMMA;
D O I：
10.1016/j.bbrc.2016.05.068
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：
Oxidized low-density lipoproteins (ox-LDL) play a critical role in endothelial injury including cytoskeleton reorganization, which is closely related to actin-related protein 2/3 (Arp2/3) complex. The aim of this study was to investigate the role of Arp2/3 complex in ox-LDL-induced endothelial dysfunction. In this study, we found that Arp2 and Arp3 expression was increased under atherosclerotic conditions both in ApoE(-/-) mice and in ox-LDL-stimulated human coronary artery endothelial cells (HCAECs). Arp2/3 complex inhibitor CK666 significantly reduced ox-LDL-induced ROS generation and cytoskeleton reorganization, and increased NO release in HCAECs. Pretreatment with LOX-1- but not CD36-blocking antibody markedly decreased ox-LDL-induced Arp2 and Arp3 expression. Moreover, Rac-1 siRNA remarkably suppressed ox-LDL-stimulated Arp2 and Arp3 expression. Additionally, CK666 reduced endothelial nitric oxide synthase (eNOS) expression and atherosclerotic lesions in ApoE(-/-) mice. Collectively, ox-LDL induces endothelial dysfunction by activating LOX-1/Rac-1 signaling and upregulating Arp2/3 complex expression. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码：182 / 188
页数：7
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