C-reactive protein upregulates complement-inhibitory factors in endothelial cells

Article

关键词: DECAY-ACCELERATING FACTOR;    VASCULAR SMOOTH-MUSCLE;    ATHEROSCLEROTIC PLAQUES;    MEDIATED INJURY;    ACTIVATION;    INFLAMMATION;    ANGIOGENESIS;    COMPONENTS;    INDUCTION;    MARKERS;   

DOI  :  10.1161/01.CIR.0000117087.27524.0E

来源: SCIE

【 摘 要 】

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.

【 授权许可】

Free