O244	Platelet adhesion, aggregation and microparticle formation on von Willebrand Factor, collagen and atherosclerotic plaques.
1A.J.Reininger, 2S.Penz, 3R.Brandl, 2W.Siess, 4Z.M.Ruggeri
1University Clinic, Department of Transfusion Medicine and Hemostaseology, München, DE; 2University Clinic, Institute for Prevention of Cardiovascular Diseases, München, DE; 3Klinikum Munich-Schwabing, Department of Vascular Surgery, München, DE; 4The Scripps Research Institute, La Jolla, US.

Platelets contribute to thrombosis under distinct hemodynamic conditions. Within stenosed coronary arteries the extreme flow velocity can lead to shear rates of 20,000-40,000 1/s. Platelet adhesion to collagen or atherosclerotic plaques from fast flowing blood requires initial immobilization of soluble von Willebrand factor (VWF) to the collagen fibers with subsequent platelet arrest via its GPIb receptors binding to VWF. By using reflection interference contrast microscopy we could visualize this process in real-time showing platelets attaching via Discrete Adhesion Points (DAPs) of their membrane with an area of only 0.1 micrometer2 that exhibits approximately 100-300 GPIb receptors. These DAPs anchored the platelet in place thus resisting shear forces of more than 160 picoNewton. However downstream movement of the platelets enforced by the flow caused passive extraction of membrane tethers. When they were eventually severed from the platelet body they formed isolated tethers and microparticles. Such platelet derived microparticles generated after milliseconds interaction of platelets with VWF exhibited tissue factor and regular platelet receptors GPIb and GPIIb/IIIa. On perfused atherosclerotic plaques the platelets adhered, aggregated and fibrin was formed, with microparticles present in the microenvironment of the thrombus. This may suggest a role for microparticles in thrombus formation.

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