Plateletadhesion

Platelet adhesion is the process by which circulating platelets first attach to sites of vascular injury, anchoring to the subendothelial matrix and to exposed collagen and other proteins. This initial adhesion precedes platelet activation and aggregation, and is essential for formation of the primary hemostatic plug.

Mechanisms involve several receptor–ligand interactions. In the high-shear environment of arteries, platelet tethering is mediated mainly by the interaction between the platelet receptor GPIb-IX-V and the plasma protein von Willebrand factor bound to exposed subendothelial collagen. The platelet receptors GPVI and integrin α2β1 also bind to collagen, promoting firm adhesion and spreading. Activation by soluble agonists such as thrombin, adenosine diphosphate (ADP), and thromboxane A2 (TXA2) induces inside-out signaling that converts integrin αIIbβ3 to a high-affinity state. While αIIbβ3 primarily mediates platelet-platelet interactions during aggregation, it also contributes to stable adhesion by binding fibrinogen and von Willebrand factor.

Platelet adhesion leads to activation and release of mediators that recruit additional platelets and amplify the response, culminating in a platelet plug. Adhesion is regulated by shear rate, endothelial cell status, and the composition of the extracellular matrix, and is coordinated with the coagulation cascade.

Clinical relevance is related to defects in adhesion pathways. Von Willebrand disease reduces vWF-mediated adhesion; Bernard-Soulier syndrome, due to deficiency of the GPIb-IX-V complex, impairs adhesion. Therapies that target adhesion pathways, including anti-platelet drugs that affect GPIIb/IIIa interactions, primarily influence aggregation but can also impact adhesion under certain conditions.