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Frontiers of Medicine >> 2019, Volume 13, Issue 6 doi: 10.1007/s11684-018-0673-5

Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via p38MAPK: a pathway to targeted therapies

. Department of Laboratory Diagnosis, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.. Department of Emergency, The First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin 150040, China

Accepted: 2019-02-28 Available online: 2019-02-28

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Abstract

Anti- glycoprotein I (anti- GPI) antibodies are important contributors to the development of thrombosis. Anti- GPI antibody complexes with GPI are well known to activate monocytes and endothelial cells via the intracellular NF- B pathway with prothrombotic implications. By contrast, the interaction of anti- GPI/ GPI complexes with platelets has not been extensively studied. The p38 mitogen-activated protein kinase (MAPK) pathway has been recognized to be an important intracellular signaling pathway in the coagulation cascade and an integral component of arterial and venous thrombosis. The present study reveals that levels of anti- GPI/ GPI complexes in sera are positively associated with p38MAPK phosphorylation of platelets in thrombotic patients. Furthermore, SB203580 inhibits anti- GPI/ GPI complex-induced platelet activation. Thrombus formation decreased in mice after treatment with anti- GPI/ GPI complexes. In conclusion, p38MAPK may be a treatment target for anti- GPI antibody-associated thrombotic events.

Keywords

anti-

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