Vascular smooth muscle cells synthesize, secrete and express coagulation factor V.
Expression of cellular procoagulant activity may be one of the more important responses to vascular injury. Because factor V, a coagulation cofactor in the prothrombinase complex, catalyzes the conversion of prothrombin to thrombin, it may be a key to understanding this response. Therefore, we have investigated the synthesis, secretion and expression of factor V by vascular smooth muscle cells, which proliferate at sites of vascular injury. Cultured aortic vascular smooth muscle cells constitutively secreted Factor V activity, as determined by a functional assay. Labeled factor V was immunoprecipitated from conditioned medium of [35S]methionine-labeled cells, indicating that the secreted factor V was synthesized by vascular smooth muscle cells. Treatment of vascular smooth muscle cells with tunicamycin prevented secretion of factor V, suggesting that its secretion was dependent on the presence of N-linked carbohydrate. Factor V activity was also expressed on the vascular smooth muscle cell surface, as indicated by the ability of cultured cells to promote factor Xa-catalyzed prothrombin activation. These data suggest that the proliferation of smooth muscle cells in response to vascular injury may be one mechanism that links vascular disease with thrombosis.
Rodgers
G M
GM
Gladstone Foundation Laboratories for Cardiovascular Disease, San Francisco General Hospital, CA 94140.
D000818:Animals; D001011:Aorta / Q000201:enzymology; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000201:enzymology; D004789:Enzyme Activation; D005165:Factor V / Q000096:biosynthesis / Q000378:metabolism*; D007700:Kinetics; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000201:enzymology*; D014415:Tunicamycin / Q000494:pharmacology
D014415:Tunicamycin; D005165:Factor V