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Platelets in hemostasis and thrombosis: role of integrins and their ligands

Heyu Ni1, John Freedman

  • 1Transfusion Medicine Research, Department of Laboratory Medicine and Pathobiology, St. Michael's Hospital, University of Toronto and the Canadian Blood Services, Toronto, Ont.,Canada M5B1W8. nih@smh.toronto.on.ca

Transfusion and Apheresis Science : Official Journal of the World Apheresis Association : Official Journal of the European Society for Haemapheresis
|May 3, 2003
PubMed

Platelet adhesion and aggregation at the site of vascular injury are two key events in hemostasis and thrombosis. The contribution of several platelet receptors and their ligands has been highlighted in these processes. In platelet adhesion, particularly at high shear stress, GP1b-von Willebrand factor (vWF) interaction may initiate this event, which is followed by firm platelet adhesion mediated by members of the integrin family, such as beta1 (alpha2beta1, alpha5beta1) and beta3 (alphaIIbbeta3) integrins. In platelet aggregation, although GP1b-vWF, P selectin-sulfatides, and other molecules, may play some roles, the process is mainly mediated by beta3 (alphaIIbbeta3) integrin and its ligands, such as fibrinogen and vWF. Recent studies with perfusion chambers and intravital microscopy have revised the dogma established with the static (low shear stress) conditions. It is intriguing that platelet adhesion and aggregation do still occur in mice lacking both vWF and fibrinogen, suggesting that other unexpected molecule(s) may also be important in hemostasis and thrombosis.

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