Participants in the 2009 Platelet Colloquium are listed in the Appendix.
Platelet functions beyond hemostasis
Version of Record online: 19 AUG 2009
© 2009 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 7, Issue 11, pages 1759–1766, November 2009
How to Cite
SMYTH, S. S., MCEVER, R. P., WEYRICH, A. S., MORRELL, C. N., HOFFMAN, M. R., AREPALLY, G. M., FRENCH, P. A., DAUERMAN, H. L., BECKER, R. C. and FOR THE 2009 PLATELET COLLOQUIUM PARTICIPANTS (2009), Platelet functions beyond hemostasis. Journal of Thrombosis and Haemostasis, 7: 1759–1766. doi: 10.1111/j.1538-7836.2009.03586.x
- Issue online: 21 OCT 2009
- Version of Record online: 19 AUG 2009
- Received 6 June 2009, accepted 30 July 2009
- immune response;
Summary. Although their central role is in the prevention of bleeding, platelets probably contribute to diverse processes that extend beyond hemostasis and thrombosis. For example, platelets can recruit leukocytes and progenitor cells to sites of vascular injury and inflammation; they release proinflammatory and anti-inflammatory and angiogenic factors and microparticles into the circulation; and they spur thrombin generation. Data from animal models suggest that these functions may contribute to atherosclerosis, sepsis, hepatitis, vascular restenosis, acute lung injury, and transplant rejection. This article represents an integrated summary of presentations given at the Fourth Annual Platelet Colloquium in January 2009. The process of and factors mediating platelet–platelet and platelet–leukocyte interactions in inflammatory and immune responses are discussed, with the roles of P-selectin, chemokines and Src family kinases being highlighted. Also discussed are specific disorders characterized by local or systemic platelet activation, including coronary artery restenosis after percutaneous intervention, alloantibody-mediated transplant rejection, wound healing, and heparin-induced thrombocytopenia.