The role of platelets in haemostasis involves the following steps: t
* Adherence: platelets adhere to the exposed subendothelial matrix (the components of which include collagen, fibronectin and von Willebrand factor) through an interaction between the glycoprotein Ib-IX-V complex on their surface and von Willebrand factor in the subendothelium. This is aided by high fluid shear stresses within the lumen secondary to vascular constriction.
* Other adhesive reactions ensue and involve platelet integrins such as the platelet glycoprotein Ilb-IIIa complex which bind subendothelial matrix components such as fibrinogen, von Willebrand factor, collagen and fibronectin. This brings about platelet-to-platelet aggregation.
* The adherence of platelets is followed by their activation.
* Platelets are activated by specific agonists, of which thrombin is probably the most important. These agonists bind to their specific receptors, G-protein-coupled receptors, in the platelet cell membrane, and trigger a cascade of intracellular signals, mediated by the sequential activation of several enzymes, including phospholipase C (which produces inositol 1,4,5-triphos-phate and 1, 2-diacylglycerol) and protein kinase C.
* Activation of protein kinase C and the generation of thromboxane A2 are crucial for the activation of the fibrinogen receptor - the IIb-IIIa complex (glycoprotein(GP)IIb/IIIa).
* Fibrinogen binds to the GPIIb/IIIa complex of adjacent platelets, mediating linkage of platelets and thereby causing them to aggregate.
Platelet plug formation thus entails the steps of surface adhesion, change in shape, degranulation and release of granule contents, aggregation, and consolidation.
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