Mechanisms Involved in Platelet Procoagulant Response

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Abstract

Blood platelets are essential to the normal hemostatic process. Vessel wall injury produces several platelet agonists which through specific membrane receptors elicit a variety of cellular responses. Shape change, activation of binding sites for fibrinogen and other adhesive molecules, and secretion of intracellular granule contents ensure the rapid formation of large platelet aggregates, which prevent further loss of blood from the injured vessel. In addition, an important platelet response is the surface exposure of specific phospholipids, providing a catalytic surface for the assembly of enzyme complexes of the coagulation cascade. This platelet procoagulant response leads to a dramatic increase in the rate of thrombin formation, which allows rapid formation of an insoluble meshwork of fibrin, required to consolidate the primary haemostatic plug. On the other hand, the same catalytic surface is also instrumental in negative feedback control of the coagulation cascade by activated protein C. Platelets are the primary source of procoagulant lipid surfaces, but other cells such as erythrocytes or endothelial cells may, sometimes, under pathological conditions- also become procoagulant.