Platelets and their membranes in hemostasis: physiology and pathophysiology.
Platelets form a plug and promote thrombin generation at sites of vascular injury. These processes are initiated by interaction of the platelet plasma membrane with various substances within or accumulating at the injured vessel. Thus, platelet adhesion to exposed subendothelium requires the binding of von Willebrand factor to platelets. Agonists such as thrombin bind to membrane receptors, thereby stimulating the binding of fibrinogen to platelets and resulting in the aggregation of platelets onto those already adherent to the vessel wall. Agonists also stimulate transfer of membrane=bound calcium into the cytoplasm. This triggers the secretion of granule substances and results in the recruitment of additional platelets to the hemostatic plug. Concomitant with secretion, the platelet surface supports several reactions leading to thrombin generation. Thus, hemostasis requires a series of coordinated responses involving platelet membranes. A defect in any of these responses can lead to a bleeding diathesis.
D001791:Blood Platelet Disorders / Q000209:etiology; D001792:Blood Platelets / Q000502:physiology* / Q000648:ultrastructure; D002462:Cell Membrane / Q000648:ultrastructure; D005337:Fibrin / Q000502:physiology; D006487:Hemostasis; D006801:Humans; D007425:Intracellular Membranes / Q000648:ultrastructure; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D010977:Platelet Factor 3 / Q000502:physiology
D010977:Platelet Factor 3; D005337:Fibrin