The Role of Transmembrane Glycoproteins, Integrins, and Serpentine Receptors in Platelet Adhesion and Activation

Platelets are unique cells of human body: they lack nucleus, are very small in size (1-2 mu m) and involved in several physiological responses, including hemostasis, immunity and angiogenesis. Platelets play a key role in the formation of primary hemostatic plug following injuries of vessels possessing high shear rate blood flow. According to a generally accepted view, a platelet response to endothelium injury under shear conditions exceeding 1000 s(-1) includes primary binding of platelet glycoprotein receptor complex GPIb-IX-V with von Willebrand factor-a huge multimeric protein of the blood plasma that specifically interacts with collagen fibers. Further stabilization of primary adhesion involves platelet activation. There are over ten membrane receptor types that trigger several signaling cascades leading to platelet cytoskeleton remodeling, granule release and activation of integrins, which are responsible for stable adhesion and platelet aggregation. This review is focused on biophysical aspects of interactions between platelet membrane glycoproteins and integrins with their basic ligands and offers the up-to-date overview of the platelet activation mechanisms that are important for stable primary adhesion of the platelets and their aggregation.