Defective Serum PGI2 Binding in Thrombotic Stroke: A Potential Mechanism for Platelet Hyperaggregability in Stroke
The blood platelet plays a pivotal role in the pathogenesis of thrombotic stroke. It contributes to the formation of atherosclerotic plugs via its interaction with damaged vessel wall and the release of platelet-derived growth factor (PDGF) from its α-granules and generation of 12-hydroxyeicosatetraenoic acid (12-HETE) via arachidonic acid metabolism. 12-HETE induces vascular smooth muscle cell migration  while PDGF stimulates its proliferation . Platelets are key elements of thrombotic plugs formed on the atherosclerotic plugs. Formation of thrombotic plugs involves multiple steps of platelet activation including adhesion, spreading, release reaction, and aggregation and the surface catalysis of coagulation. Multiple chemical reactions are activated to initiate and reinforce these biological processes. This subject is beyond the scope of this paper and readers are referred to review articles . It is sufficient to emphasize that thrombotic plugs and the detached debris are the major factors contributing to the acute cerebrovascular events.
KeywordsStroke Patient Platelet Activation Thrombotic Thrombocytopenic Purpura Maximal Binding Capacity Vascular Smooth Muscle Cell Migration
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