Anti-β2 glycoprotein I （anti-β2GP I） antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome （APS）. However, the mechanism by which anti-β2GP I antibodies are ...Anti-β2 glycoprotein I （anti-β2GP I） antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome （APS）. However, the mechanism by which anti-β2GP I antibodies are involved in the pathogenesis of thrombosis is not fully understood. In this report, we investigated the role of anti- β2GP I antibodies in complexes with β2GP I as mediators of platelet activation, which can serve as a potential source contributing to thrombosis. We examined the involvement of the apolipoprotein E receptor 2＇ （apoER2＇） and glycoprotein I ba （GP I bα） in platelet activation induced by the anti-β2GP I/β2GP I complex. The interaction between the anti-β2GP I/β2GP I complex and platelets was examined using in vitro methods, in which the Fc portion of the antibody was immobilized using protein A coated onto a microtiter plate. Platelet activation was assessed by measuring GP II b/III a activation and F-selectin expression and thromboxane B2 production as well as p38 mitogen-activated protein kinase phosphorylation. Our results revealed that the anti-β2GPI/β2GPI complex was able to activate platelets, and this activation was inhibited by either the anti-GP I bα antibody or the apoER2＇ inhibitor. Results showed that the anti-β2GPI/β2GPl complex induced platelet activation via GP I bα and apoER2＇, which may then contribute to the prothrombotic tendency in APS patients.展开更多
基金This work was supported by the National Natural Science Foundation of China （No. 81270394） to Yanhong Liu. The authors would like to thank Xing Liu for providing expert technical assistance.
文摘Anti-β2 glycoprotein I （anti-β2GP I） antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome （APS）. However, the mechanism by which anti-β2GP I antibodies are involved in the pathogenesis of thrombosis is not fully understood. In this report, we investigated the role of anti- β2GP I antibodies in complexes with β2GP I as mediators of platelet activation, which can serve as a potential source contributing to thrombosis. We examined the involvement of the apolipoprotein E receptor 2＇ （apoER2＇） and glycoprotein I ba （GP I bα） in platelet activation induced by the anti-β2GP I/β2GP I complex. The interaction between the anti-β2GP I/β2GP I complex and platelets was examined using in vitro methods, in which the Fc portion of the antibody was immobilized using protein A coated onto a microtiter plate. Platelet activation was assessed by measuring GP II b/III a activation and F-selectin expression and thromboxane B2 production as well as p38 mitogen-activated protein kinase phosphorylation. Our results revealed that the anti-β2GPI/β2GPI complex was able to activate platelets, and this activation was inhibited by either the anti-GP I bα antibody or the apoER2＇ inhibitor. Results showed that the anti-β2GPI/β2GPl complex induced platelet activation via GP I bα and apoER2＇, which may then contribute to the prothrombotic tendency in APS patients.
