Abstract
Integrins and other families of cell adhesion receptors are responsible for platelet adhesion and aggregation, which are essential steps for physiological haemostasis, as well as for the development of thrombosis. The modulation of platelet adhesive properties is the result of a complex pattern of inside-out and outside-in signaling pathways, in which the members of the Rap family of small GTPases are bidirectionally involved. This paper focuses on the regulation of the main Rap GTPase expressed in circulating platelets, Rap1b, downstream of adhesion receptors, and summarizes the most recent achievements in the investigation of the function of this protein as regulator of platelet adhesion and thrombus formation.
Highlights
The adhesion of circulating blood platelets to the subendothelial matrix exposed upon vessel wall injury represents the initial event of the haemostatic process required to limit hemorrhage
Integrins and other families of cell adhesion receptors are responsible for platelet adhesion and aggregation, which are essential steps for physiological haemostasis, as well as for the development of thrombosis
This paper focuses on the regulation of the main Rap GTPase expressed in circulating platelets, Rap1b, downstream of adhesion receptors, and summarizes the most recent achievements in the investigation of the function of this protein as regulator of platelet adhesion and thrombus formation
Summary
The adhesion of circulating blood platelets to the subendothelial matrix exposed upon vessel wall injury represents the initial event of the haemostatic process required to limit hemorrhage. Characteristic of small arteries and stenotic vessels, platelets are unable to efficiently interact to exposed collagen fibers, and in these conditions adhesion is preceded by platelet tethering and rolling on the site of injury This process is mediated by the membrane GPIb-IX-V complex, a platelet-specific receptor for the multimeric glycoprotein von Willebrand factor (VWF). The interaction of platelet adhesion receptors with subendothelial matrix components stimulates an intricate pattern of signal transduction pathways, that trigger spreading, secretion of soluble proaggregating molecules, thromboxane A2 (TxA2) synthesis and release, and phosphatydilserine exposure These events recruit and activate additional circulating platelets to initiate a process of cell aggregation, that generates a rapidly growing thrombus at the site of damaged vessel wall. This paper will focus on platelet Rap GTPases to highlight recent insights into the mechanism of activation and recruitment upon stimulation of the major platelet adhesion receptors
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