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Prepublished online as a Blood First Edition Paper on February 20, 2003; DOI 10.1182/blood-2002-09-2944.
Submitted September 26, 2002
Accepted February 1, 2003
Identification of Thrombin Activatable Fibrinolysis Inhibitor (TAFI) in human platelets
Laurent O Mosnier*, Paula Buijtenhuijs, Pauline F Marx, Joost C M Meijers, and Bonno N Bouma
Thrombosis and Haemostasis Laboratory, Department of Haematology, University Medical Center Utrecht, Utrecht, The Netherlands
Institute of Biomembranes, Utrecht University, Utrecht, The Netherlands
Department of Vascular Medicine, Academical Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Department Molecular and Experimental Medicine, The Scripps research Institute, La Jolla, CA, USA
* Corresponding author; email: lmosnier{at}scripps.edu.
Thrombin Activatable Fibrinolysis Inhibitor (TAFI) is a carboxypeptidase B-like proenzyme that after activation downregulates fibrinolysis. Platelets are known to contain anti-fibrinolytic factors that are secreted during platelet activation. Therefore, the presence of TAFI in platelets was analyzed. TAFI was identified in platelets in a concentration of about 50 ng/1*109 platelets and was secreted upon platelet activation. Thrombin-mediated activation of platelet-derived TAFI resembled that of plasma-derived TAFI with respect to stimulation by thrombomodulin and spontaneous loss of activity at 37°C. The different glycosylation of platelet-derived TAFI compared to plasma-derived TAFI suggest that platelet-derived TAFI is synthesized in the megakaryocyte. This was substantiated by the detection of mRNA in the megakaryocytic cell lines DAMI and CHRF, representing the intermediate and late stages of megakaryocyte development. These results establish the presence of TAFI in platelets and suggest a role for platelet-derived TAFI in the protection of the clot against fibrinolysis.
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