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

Chiara Cerletti; Virgilio Evangelista; Giovanni de Gaetano

doi:10.1055/s-0037-1615912

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 1999; 82(02): 787-793
DOI: 10.1055/s-0037-1615912

Research Article

Schattauer GmbH

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

Authors

Chiara Cerletti

¹G. Bizzozero Laboratory of Platelet and Leukocyte Pharmacology, Santa Maria Imbaro, ITALY
Virgilio Evangelista

¹G. Bizzozero Laboratory of Platelet and Leukocyte Pharmacology, Santa Maria Imbaro, ITALY

²Unit of Biology of Cell Interactions, Consorzio Mario Negri Sud, Santa Maria Imbaro, ITALY
Giovanni de Gaetano

Istituto di Ricerche Farmacologiche Mario Negri, Department of Vascular Medicine and Pharmacology, Santa Maria Imbaro, ITALY

Abstract

Introduction

Platelets activated at the site of vascular damage play a pivotal role in polymorphonuclear (PMN) leukocyte accumulation in a growing thrombus^2,3 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.

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Referenzen

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