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

MCP-induced protein 1 suppresses TNFalpha-induced VCAM-1 expression in human endothelial cells.
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DOI:
10.1016/j.febslet.2010.05.040
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发表时间:
2010-07-16
期刊:
影响因子:
3.5
通讯作者:
Fu M
Fu M
中科院分区:
生物学3区
文献类型:
--
作者:
Qi Y;Liang J;She ZG;Cai Y;Wang J;Lei T;Stallcup WB;Fu M

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内皮炎症在心血管疾病的发生和发展中起着至关重要的作用,尽管其机制需要充分阐明。我们在此报道用肿瘤坏死因子(TNF)α处理人脐静脉内皮细胞(HUVECs)显著增加MCP诱导蛋白1(MCPIP 1)的表达。MCPIP 1的过表达可保护EC免受TNFα诱导的内皮活化,其特征在于粘附分子VCAM-1的表达和单核细胞粘附EC的减弱。相反,小干扰RNA介导的MCPIP 1敲低增加了VCAM-1的表达和单核细胞对EC的粘附。这些研究将MCPIP 1鉴定为细胞因子诱导的内皮炎症的反馈控制。
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.
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