Platelets in hemostasis and thrombosis: role of integrins and their ligands

Abstract

Platelet adhesion and aggregation at the site of vascular injury are two key events in hemostasis and thrombosis. The contribution of several platelet receptors and their ligands has been highlighted in these processes. In platelet adhesion, particularly at high shear stress, GP1b–von Willebrand factor (vWF) interaction may initiate this event, which is followed by firm platelet adhesion mediated by members of the integrin family, such as β1 (α2β1, α5β1) and β3 (αIIbβ3) integrins. In platelet aggregation, although GP1b–vWF, P selectin-sulfatides, and other molecules, may play some roles, the process is mainly mediated by β3 (αIIbβ3) integrin and its ligands, such as fibrinogen and vWF. Recent studies with perfusion chambers and intravital microscopy have revised the dogma established with the static (low shear stress) conditions. It is intriguing that platelet adhesion and aggregation do still occur in mice lacking both vWF and fibrinogen, suggesting that other unexpected molecule(s) may also be important in hemostasis and thrombosis.