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Anti-β 2 GPI/β 2 GPI complexes induce platelet activation and promote thrombosis via p38MAPK: a pathway to targeted therapies.

Frontiers of Medicine 2019 Februrary 29
Anti-β2 glycoprotein I (anti-β2 GPI) antibodies are important contributors to the development of thrombosis. Anti-β2 GPI antibody complexes with β2 GPI are well known to activate monocytes and endothelial cells via the intracellular NF-kB pathway with prothrombotic implications. By contrast, the interaction of anti- β2 GPI/β2 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- β2 GPI/β2 GPI complexes in sera are positively associated with p38MAPK phosphorylation of platelets in thrombotic patients. Furthermore, SB203580 inhibits anti-β2 GPI/β2 GPI complex-induced platelet activation. Thrombus formation decreased in p38MAPK-/- mice after treatment with anti-β2 GPI/β2 GPI complexes. In conclusion, p38MAPK may be a treatment target for anti-β2 GPI antibody-associated thrombotic events.

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