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Circulation. 2004 Feb 24;109(7):833-6. Epub 2004 Feb 16.

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

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  • 1Division of Cardiac Surgery, Toronto General Hospital, Toronto, Ontario, Canada.

Abstract

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 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.

CONCLUSIONS:

These observations provide evidence for a possible protective role for CRP in atherogenesis.

PMID:
14967730
[PubMed - indexed for MEDLINE]
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