P-Selectin-β2-Integrin Cross-Talk: A Molecular Mechanism For Polymorphonuclear Leukocyte Recruitment At The Site Of Vascular Damage

Abstract

IntroductionPlatelets activated at the site of vascular damage play a pivotal role in polymorphonuclear (PMN) leukocyte accumulation in a growing thrombus2,3 and may substitute endothelial cells in the recruitment and migration of leukocytes through damaged vessel wall.4 Leukocytes, accumulated in a platelet thrombus, can contribute to further platelet activation5 and to increased fibrin deposition.6 These events, on the one hand, may contribute to the maintenance of vascular and tissue integrity. They may, however, play a pathogenic role in inflammatory and thrombotic disease, providing some biological plausibility to the epidemiological evidence of significant association between leukocyte count and the incidence of coronary heart disease.7,8 We shall focus our attention on the molecular mechanisms involved in the recruitment of PMN leukocytes on activated platelets as it occurs at the site of vascular damage, with particular attention to P-selectin- β2-integrin cross-talk.