They aggregate upon activation, forming a thrombus which serves to plug the loss of blood from a damaged blood vessel. Platelets can be activated by many ligands, but collagens of the blood vessel wall are the primary physiological agonists. This event is the major cause of death in the western world. Platelets also participate in blood coagulation, as the activation process leads to the expression of phosphatidylserine, particularly, on the platelet surface which is essential for catalysing the conversion of prothrombin to thrombin.
Thrombin stimulates blood coagulation, but is also a potent platelet agonist.
Work in this laboratory is directed towards a detailed understanding of the platelet-collagen interaction, in terms of both the reactive amino acid sequences within the various collagen types, and the platelet receptors which recognise these sequences. A specific interest is the role of each particular collagen receptor in the platelet activation process. Activation can be seen as platelet aggregation, induction of intracellular signalling steps, morphological changes, microvesiculation and procoagulant activity. This research will lead to the rational development of antagonists of the platelet-collagen interaction which may be used to prevent thrombosis. Tyrosine kinase activation, including of fak, syk, src, MAP kinases.