C-reactive protein upregulates complement-inhibitory factors in endothelial cells
C-reactive protein upregulates complement-inhibitory factors in endothelial cells
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DOI：
10.1161/01.cir.0000117087.27524.0e
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发表时间：
2004-02-24
期刊：
影响因子：
37.8
通讯作者：
Verma, S
中科院分区：
文献类型：
--
作者：
Li, SH;Szmitko, PE;Verma, S
背景-由于补体介导的血管损伤参与动脉粥样硬化，而C-反应蛋白(CRP)可以激活补体级联反应，我们试图确定CRP是否影响内皮细胞(ECs)细胞表面保护性补体抑制因子的表达。方法和结果：将人冠状动脉或人大隐静脉内皮细胞与CRP(0~100µg/mL，0~72小时)孵育，用流式细胞仪检测补体抑制蛋白衰变加速因子(DAF)、膜辅助因子蛋白(CD46)和CD59的表达。与CRP共同孵育后，3种蛋白的表达均显著增加。C反应蛋白诱导的DAF上调需要增加稳态mRNA和从头合成蛋白质。补体抑制蛋白表达的增加在功能上是有效的，导致抗体包被的人隐静脉内皮细胞补体介导的裂解作用显著减少。结论：这些观察结果为CRP在动脉粥样硬化形成中可能的保护作用提供了证据。
Background - Because complement-mediated vascular injury participates in atherosclerosis and C-reactive protein (CRP) can activate the complement cascade, we sought to determine whether CRP affects the expression of the protective complement-inhibitory factors on the cell surface of endothelial cells (ECs).Methods and Results - Human coronary artery or human saphenous vein ECs were incubated with CRP ( 0 to 100 mug/mL, 0 to 72 hours), and the expression of the complement-inhibitory proteins decay-accelerating factor (DAF), membrane cofactor protein (CD46), and CD59 were measured by flow cytometry. Incubation with CRP resulted in a significant increase in the expression of all 3 proteins. CRP-induced upregulation of DAF required increased steady-state mRNA and de novo protein synthesis. The increased expression of complement-inhibitory proteins was functionally effective, resulting in significant reduction of complement-mediated lysis of antibody-coated human saphenous vein ECs.Conclusions - These observations provide evidence for a possible protective role for CRP in atherogenesis.