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Blood, 1 September 2007, Vol. 110, No. 5, pp. 1483-1491. Prepublished online as a Blood First Edition Paper on May 8, 2007; DOI 10.1182/blood-2006-10-053199.
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY ß2-Glycoprotein I inhibits von Willebrand factor–dependent platelet adhesion and aggregation1 Laboratory for Thrombosis and Haemostasis, Department of Clinical Chemistry and Haematology; 2 Department of Rheumatology and Clinical Immunology, University Medical Centre Utrecht, Utrecht; 3 Jeroen Bosch Hospital, Department of Internal Medicine, Hertogenbosch, the Netherlands
Patients with antiphospholipid syndrome are characterized by the association of thrombosis or pregnancy morbidity and the presence of antiphospholipid autoantibodies. Particularly, anti-ß2-glycoprotein (ß2 GPI) autoantibodies correlate with thrombosis, suggesting an antibody-induced gain of prothrombotic function and/or an antibody-induced loss of antithrombotic function of ß2 GPI. In the search for potential antithrombotic properties of ß2 GPI, we found that ß2 GPI inhibits von Willebrand factor (VWF)–induced platelet aggregation. In addition, platelet adhesion to a VWF-coated surface was decreased by 50% in the presence of ß2 GPI (P < .03). ß2 GPI binds to the A1 domain of VWF but preferably when the A1 domain is in its active glycoprotein Ib
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