Li Shu-Hong, Szmitko Paul E, Weisel Richard D, Wang Chao-Hung, Fedak Paul W M, Li Ren-Ke, Mickle Donald A G, Verma Subodh
Division of Cardiac Surgery, Toronto General Hospital, Toronto, Ontario, Canada.
Circulation. 2004 Feb 24;109(7):833-6. doi: 10.1161/01.CIR.0000117087.27524.0E. Epub 2004 Feb 16.
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).
Human coronary artery or human saphenous vein ECs were incubated with CRP (0 to 100 microg/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.
These observations provide evidence for a possible protective role for CRP in atherogenesis.
由于补体介导的血管损伤参与动脉粥样硬化的发生，且C反应蛋白（CRP）可激活补体级联反应，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。
将人冠状动脉或人隐静脉内皮细胞与CRP（0至100μg/mL，0至72小时）孵育，通过流式细胞术检测补体抑制蛋白衰变加速因子（DAF）、膜辅因子蛋白（CD46）和CD59的表达。与CRP孵育导致这3种蛋白的表达显著增加。CRP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具有功能效应，导致补体介导的抗体包被的人隐静脉内皮细胞溶解显著减少。
这些观察结果为CRP在动脉粥样硬化发生中可能具有的保护作用提供了证据。
