期刊
FEBS LETTERS
卷 584, 期 14, 页码 3065-3072出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2010.05.040
关键词
MCPIP1; Endothelial cell; Inflammation; NF-kappa B signaling; Adhesion molecule
资金
- American Heart Association [09BGIA2460030]
- James and Ester King Biomedical Research Grant [08KN-03]
- National Natural Science Foundation of China [30470693]
- State Major Basic Research Development Program of the People's Republic of China [2006CB503807]
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.
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