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C反应蛋白(CRP)通过磷脂酰肌醇-3激酶(PI3-激酶)和细胞外信号调节激酶1/2(ERK 1/2)依赖的信号通路增加单核细胞中血管内皮生长因子A(VEGF-A)的表达。

C-reactive protein (CRP) increases VEGF-A expression in monocytic cells via a PI3-kinase and ERK 1/2 signaling dependent pathway.

作者信息

Bello Gaëlle, Cailotto Frédéric, Hanriot Didier, Kolopp-Sarda Marie-Nathalie, Latger-Cannard Véronique, Hess Ketsia, Zannad Faiez, Longrois Dan, Ropars Armelle

机构信息

INSERM, U684, Vandoeuvre les Nancy, F-54500 France.

出版信息

Atherosclerosis. 2008 Oct;200(2):286-93. doi: 10.1016/j.atherosclerosis.2007.12.046. Epub 2008 Feb 15.

DOI:10.1016/j.atherosclerosis.2007.12.046
PMID:18280482
Abstract

C-reactive protein (CRP) is an independent predictor of atherosclerosis and its complications. Monocytes/macrophages are implicated in this complex disease which is, among other mechanisms, characterised by angiogenesis. The aim of this study was to analyse whether CRP plays a role in VEGF-A regulation by monocytic cells. Our findings show that CRP up-regulates VEGF-A mRNA expression and protein excretion in THP-1 cells in a concentration- and time-dependent manner. Furthermore, we studied the signaling pathway underlying this effect. CRP increases VEGF-A expression via a PI3-kinase and an extracellular-signal-regulated kinase (ERK) 1/2 dependent pathway. Our results suggest that CRP could play a role in the angiogenesis process via immune cells such as monocytes.

摘要

C反应蛋白(CRP)是动脉粥样硬化及其并发症的独立预测指标。单核细胞/巨噬细胞参与了这种复杂疾病,该疾病在其他机制中以血管生成特征。本研究的目的是分析CRP是否在单核细胞对血管内皮生长因子A(VEGF-A)的调节中发挥作用。我们的研究结果表明,CRP以浓度和时间依赖性方式上调THP-1细胞中VEGF-A mRNA表达和蛋白分泌。此外,我们研究了这种效应背后的信号通路。CRP通过磷脂酰肌醇-3激酶(PI3-激酶)和细胞外信号调节激酶(ERK)1/2依赖性途径增加VEGF-A表达。我们的结果表明,CRP可能通过单核细胞等免疫细胞在血管生成过程中发挥作用。

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