The relative importance of platelet integrins in hemostasis, thrombosis and beyond

Integrins are heterodimeric transmembrane receptors composed of & alpha; and & beta; chains, with an N-terminal extracellular do-main forming a globular head corresponding to the ligand binding site. Integrins regulate various cellular functions in-cluding adhesion, migration, proliferation, spreading and apoptosis. On platelets, integrins play a central role in adhesion and aggregation on subendothelial matrix proteins of the vascular wall, thereby ensuring hemostasis. Platelet integrins belong either to the & beta;1 family (& alpha;2 & beta;1, & alpha;5 & beta;1 and & alpha;6 & beta;1) or to the & beta;3 family (& alpha;IIb & beta;3 and & alpha;v & beta;3). On resting platelets, integrins can engage their ligands when the latter are immobilized but not in their soluble form. The effects of various agonists promote an inside-out signal in platelets, increasing the affinity of integrins for their ligands and conveying a modest signal reinforcing platelet activation, called outside-in signaling. This outside-in signal ensures platelet adhesion, shape change, granule secretion and aggregation. In this review, we examine the role of each platelet integrin in hemostatic plug formation, hemostasis and arterial thrombosis and also beyond these classical functions, notably in tumor metastasis and sepsis.

Automated summary

Integrins are transmembrane receptors composed of alpha and beta chains, regulating various cellular functions, including adhesion, migration, proliferation, spreading, and apoptosis. Platelet integrins play a central role in hemostasis by adhesion and aggregation on vascular matrix proteins. Integrins can engage ligands when immobilized, and agonists promote an inside-out signal that increases integrin affinity, reinforcing platelet activation. This review examines the role of platelet integrins in hemostatic plug formation, arterial thrombosis, tumor metastasis, and sepsis.