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MCP‐induced protein 1 suppresses TNFα‐induced VCAM‐1 expression in human endothelial cells
Author(s) -
Qi Yongfen,
Liang Jian,
She Zhi-Gang,
Cai Yan,
Wang Jing,
Lei Tianhua,
Stallcup William B.,
Fu Mingui
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.05.040
Subject(s) - vcam 1 , umbilical vein , tumor necrosis factor alpha , inflammation , small interfering rna , cell adhesion molecule , monocyte , microbiology and biotechnology , chemistry , icam 1 , cell adhesion , cancer research , adhesion , immunology , biology , rna , biochemistry , in vitro , gene , organic chemistry
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) α substantially increased the expression of MCP‐induced protein 1 (MCPIP1). Overexpression of MCPIP1 protected ECs against TNFα‐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.