Vascular smooth muscle cells synthesize,secrete and express coagulation factor V |
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| Affiliation: | 1. Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands;2. Janssen Research & Development, Titusville, NJ, USA;3. Clinical Pharmacology, Bayer Pharma AG, Wuppertal, Germany;4. Bayer HealthCare Pharmaceuticals, Montville, NJ, USA;5. Brigham and Women''s Hospital, Boston, MA, USA;6. Clinical Pharmacology Unit, Janssen Research & Development, Antwerp, Belgium;7. Duke University Medical Center, Durham, NC, USA;8. The Thrombosis and Atherosclerosis Research Institute, McMaster University, Hamilton, Ontario, Canada;1. Department of Health Sciences, Università del Piemonte Orientale, Novara, Italy;2. Department of Translational Medicine, Università del Piemonte Orientale, Novara, Italy;3. Department of Oncology, University of Torino, Torino, Italy;4. Candiolo Cancer Institute‐FPO, IRCCS, Candiolo, Torino, Italy;1. Research and Development Pharmaceuticals, Bayer AG, Wuppertal, Germany;2. CRS Clinical Research Services Wuppertal GmbH, Wuppertal, Germany |
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| Abstract: | 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. |
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