The molecular mechanisms of platelet activation in patients with cerebrovascular disease

Abstract

Cerebrovascular diseases are the second leading cause of mortality and are one of the most impor tant medical and social problems. After the damage of the vascular wall endothelial cells secrete von Wille brand factor that binds to its receptor, glycoprotein GP Ib V IX, on the platelet surface. There are two known GP Ibα gene polymorphisms, Thr145Met and T(-5)C, associated with the risk of the development of arterial thrombosis and there are differences in the expression profile of platelets from patients with various courses of coronary heart disease. The aim of this study was to determine the role of the platelet receptor for von Will ebrand factor in platelet activation in patients with cerebrovascular disease. The study included 123 patients with cerebrovascular disease and 97 healthy volunteers; in their platelets the following parameters were ana lyzed: the level of von Willebrand factor receptor by flow cytometry, the presence of GP Ibα polymorphisms Thr145Met and T(-5)C by PCR followed by subsequent restriction analysis, the level of GP Ibα gene expres sion by real time PCR, and ADP induced aggregation according to Born. We have shown that: (1) the poly morphic allele 145Met GP Ibα is more common in patients with ischemic stroke followed on macroangiop athy of cerebral vessels; (2) in activated platelets GP Ibα pre mRNA is converted into mature mRNA, and this process is blocked by administration antiplatelet agents (e.g. acetylsalicylic acid).

Platelet-mimetic strategies for modulating the wound environment and inflammatory responses

“…8 The A1 domain of the secreted VWF interacts with GPIba, a ligand-binding protein within the glycoprotein GP-Ib-V-IX complex on the platelet's surface, allowing the platelets to adhere to the damaged vascular wall. [9][10][11] GPIba also allows platelets to activate under high-shear conditions, which facilitates platelet aggregation at wound sites. 10 The activated platelets then spread along the wall and adhere to each other, forming a platelet plug to stem initial blood loss.…”