Procoagulant Albumin Increases Vascular Endothelial Cell Prostacyclin Secretion

Abstract

SummaryVascular endothelium regulates multiple aspects of platelet function through secretion of a variety of substances, including von Willebrand factor, nitric oxide, and prostacyclin (PGI2). The objective of this study was to determine whether procoagulant albumin (P-AI), a modified form of albumin present in normal human plasma could modulate endothelial cell secretion of these substances. P-AI did not affect constitutive secretion of von Willebrand factor or nitric oxide, but did increase PGI2 secretion in a time- and concentration-dependent manner. Pretreatment of endothelial cells with aspirin, or use of suramin, a broad- specificity inhibitor, prevented the response to P-AI. Prostaglandin H synthase-2 contributed to the P-AI-induced PGI2 secretion. These results indicate that in addition to inducing tissue factor activity and reducing protein C activation and fibrinolysis, P-AI also modulates vascular endothelial cell PGI2 secretion, and potentially, platelet function.