Published online before print September 21, 2006, doi: 10.1161/01.ATV.0000246775.14471.26
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© 2006 American Heart Association, Inc.
Brief Reviews |
Procoagulant Microparticles
Disrupting the Vascular Homeostasis Equation?
From Université Louis Pasteur (O.M., F.T., B.H., B.B., J.-M.F.), Faculté de Médecine, Institut d’Hématologie et d’Immunologie, Strasbourg, France; Hôpitaux Universitaires de Strasbourg (O.M., B.B.), Fédération de Cardiologie, Strasbourg, France; INSERM (O.M., F.T., B.H., B.B., J.-M.F.), U.770, Le Kremlin-Bicêtre, France; Université Paris-Sud 11 (F.T.), Faculté de Médecine, Le Kremlin-Bicêtre, France; INSERM (L.C.-J., F.D.-G.), U.608, Marseille, France; Université de la Méditerranée (L.C.-J., F.D.-G.), Faculté de Pharmacie, Marseille, France; Hôpital de la Conception (L.C.-J., F.D.-G.), Laboratoire d’Hématologie, Marseille, France.
Correspondence to Jean-Marie Freyssinet, Institut d’Hématologie et d’Immunologie, Faculté de Médecine, 4, rue Kirschleger 67085 Strasbourg Cedex, France. E-mail Jean-Marie.Freyssinet{at}hemato-ulp.u-strasbg.fr
Apoptosis and vascular cell activation are main contributors to the release of procoagulant microparticles (MPs), deleterious partners in atherothrombosis. Elevated levels of circulating platelet, monocyte, or endothelial-derived MPs are associated with most of the cardiovascular risk factors and appear indicative of poor clinical outcome. In addition to being a valuable hallmark of vascular cell damage, MPs are at the crossroad of atherothrombosis processes by exerting direct effects on vascular or blood cells. Under pathological circumstances, circulating MPs would support cellular cross-talk leading to vascular inflammation and tissue remodeling, endothelial dysfunction, leukocyte adhesion, and stimulation. Exposed membrane phosphatidylserine and functional tissue factor (TF) are 2 procoagulant entities conveyed by circulating MPs. At sites of vascular injury, P-selectin exposure by activated endothelial cells or platelets leads to the rapid recruitment of MPs bearing the P-selectin glycoprotein ligand-1 and blood-borne TF, thereby triggering coagulation. Within the atherosclerotic plaque, sequestered MPs constitute the main reservoir of TF activity, promoting coagulation after plaque erosion or rupture. Lesion-bound MPs, eventually harboring proteolytic and angiogenic effectors are additional actors in plaque vulnerability. Pharmacological strategies aimed at modulating the release of procoagulant MPs appear a promising therapeutic approach of both thrombotic processes and bleeding disorders.
Plasma membrane-derived microparticles are at the crossroad of atherothrombosis processes involving vascular inflammation, remodeling, endothelial dysfunction, and plaque thrombogenicity. After plaque disruption, trapped and circulating microparticles provide the concentration of tissue factor allowing blood coagulation to be triggered. The pharmacological modulation of microparticle release appears a promising preventive approach.
Key Words: microvesicles • phosphatidylserine • tissue factor
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