Circulating microparticles in cardiovascular disease: implications for atherogenesis and atherothrombosis.

The complex and multifactorial nature of atherogenesis and development of atherothrombotic complications involves numerous interactions between various cell types inside the vascular wall (e.g. macrophages and smooth muscle cells) and in the blood (e.g. leukocytes and platelets). One relatively recent advance in this area is the discovery of circulating microparticles and their role in endothelial damage, platelet activation, hypercoagulability and regulation of inter-cellular interactions. Microparticles are small anucleoid phospholipid vesicles released from different cells, such as platelets, erythrocytes, leukocytes and endothelial cells. Microparticles carry surface proteins and include cytoplasmic material of the parental cells responsible for the exertion of microparticle-mediated biological effects. About 25% of the procoagulant activity of stimulated platelet suspensions is associated with microparticles released upon platelet activation and their surface may be approximately 50-100-fold more procoagulant than the surface of activated platelets per se. The available lines of evidence indicate that shedding of microparticles from the parental cells is not just a passive process accompanying cellular dysfunction and apoptosis, but a tightly regulated mechanism implicated in the interactions between various cell types. The role of microparticles as biological messengers is supported by their differential and specific involvement in the pathophysiology of different cardiovascular disorders, including atherogenesis and thrombosis.