Anti-β2 glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two receptors： apolipoprotein E receptor 2＇ and glycoprotein I ba  

作　　者：Wenjing Zhang Fei Gao Donghe Lu Na Sun Xiaoxue Yin Meili Jin Yanhong Liu 

机构地区：[1]Department of Laboratory Diagnosis, the Second Affifiated Hospital of Harbin Medical University, Harbin 150086, China

出　　处：《Frontiers of Medicine》2016年第1期76-84,共9页医学前沿（英文版）

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.

摘　　要：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.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.

关 键 词：anti-β2GP I/β2GP I complex PLATELET GP I bα apoER2＇ THROMBOSIS 

分 类 号：Q592.1[生物学—生物化学] Q548.1