Platelet Adhesion

Abstract

Platelet adhesion and ensuing thrombus formation play a central role in normal hemostasis as well as in the pathogenesis of acute coronary syndromes and thrombotic disorders. Circulating blood platelets adhere to sites of vascular injury through specific adhesion receptors despite the hemodynamic forces in flowing blood that oppose adhesion contacts. At high shear, this process is initiated by the reversible interaction between the platelet membrane glycoprotein (GP)Ib-IX-V complex and von Willebrand factor (vWF) bound to subendothelial components, following disruption of the endothelial cell lining of a blood vessel. Unique biomechanical properties of the GPIb-IX-V/vWF interaction permit the initial capture of platelets under high shear flow conditions (1,2). Once tethered to the vessel wall, platelets form irreversible adhesion bonds through the interaction of platelet receptors with specific subendothelial matrix proteins and plasma proteins immobilized at the site of injury. In addition to mediating platelet adhesion, platelet receptors trigger intracellular signaling events that lead to platelet activation and the conversion of surface integrin αIIbβ3 into a form that is competent to bind soluble adhesive ligands such as plasma vWF and fibrinogen, which facilitate the crosslinking (aggregation) and further activation of platelets, providing strength and stability to the growing thrombus. The formation of a platelet plug stabilized by an insoluble fibrin network serves to prevent further blood loss from a damaged vessel.KeywordsPlatelet AggregationPlatelet ActivationHuman PlateletPlatelet AdhesionPlatelet GlycoproteinThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.