MCP-induced protein 1 suppresses TNFα-induced VCAM-1 expression in human endothelial cells

被引：41
|
作者：
Qi, Yongfen [3 ,4 ]
Liang, Jian [3 ]
She, Zhi-Gang [5 ]
Cai, Yan [4 ]
Wang, Jing [3 ]
Lei, Tianhua [3 ]
Stallcup, William B. [5 ]
Fu, Mingui [1 ,2 ,3 ]
机构：
[1] Univ Missouri, Sch Med, Shock Trauma Res Ctr, Kansas City, MO 64108 USA
[2] Univ Missouri, Sch Med, Dept Basic Med Sci, Kansas City, MO 64108 USA
[3] Univ Cent Florida, Coll Med, Burnett Sch Biomed Sci, Orlando, FL 32816 USA
[4] Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100192, Peoples R China
[5] Sanford Burnham Med Res Inst, Ctr Canc, La Jolla, CA USA
来源：
FEBS LETTERS | 2010年 / 584卷 / 14期
基金：
中国国家自然科学基金;
关键词：
MCPIP1; Endothelial cell; Inflammation; NF-kappa B signaling; Adhesion molecule; MONOCYTE CHEMOATTRACTANT PROTEIN-1; KAPPA-B; PROINFLAMMATORY ACTIVATION; TRANSCRIPTION FACTOR; MESSENGER-RNA; ATHEROSCLEROSIS; REGULATOR; REVEALS; MICE;
D O I：
10.1016/j.febslet.2010.05.040
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：
Endothelial inflammation plays a critical role in the development and progression of cardiovascular disease, albeit the mechanisms need to be fully elucidated. We here report that treatment of human umbilical vein endothelial cells (HUVECs) with tumor necrosis factor (TNF) alpha substantially increased the expression of MCP-induced protein 1 (MCPIP1). Overexpression of MCPIP1 protected ECs against TNF alpha-induced endothelial activation, as characterized by the attenuation in the expression of the adhesion molecule VCAM-1 and monocyte adherence to ECs. Conversely, small interfering RNA-mediated knock down of MCPIP1 increased the expression of VCAM-1 and monocytic adherence to ECs. These studies identified MCPIP1 as a feedback control of cytokines-induced endothelial inflammation. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：3065 / 3072
页数：8
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