Dying for attention: Microparticles and angiogenesis

See article by Brill et al.[18](pages 30–38) in this issue. Microparticles, which were initially described as cell dust, have revealed over the past few years several exciting and unexpected properties. Microparticles are submicron vesicles shed from plasma membranes following cell activation or apoptosis, whose protein and lipid profile may be considered as a snapshot of the phenotype of the cell they stem from. The molecular mechanisms of microparticle formation and shedding are not yet fully understood, but seem to involve the changes in the cytoskeleton and exposure of phosphatidylserine on the outer leaflet of the plasma membrane [1,2]. Nevertheless, microparticles can easily be generated in vitro from aggregating platelets or from cultured cells following activation or apoptosis. Microparticles are also found circulating in the blood. Their numbers increase in patients exhibiting hypercoagulability and decrease in those with bleeding disorders [2,3]. Presence of microparticles has also been documented at sites of inflammation such as the acellular lipid core of the atherosclerotic plaque or the synovial fluid from patients with rheumatoid arthritis [3–6]. Furthermore, increased numbers of circulating microparticles have been reported in patients with acute coronary syndromes or other cardiovascular diseases [2,3,7]. Although platelet-derived microparticles appear to be a significant part of the number of circulating shed membrane vesicles, particles from other cell type such as red blood cells, leukocytes, or endothelial cells also contribute to the plasmatic pool. For example, circulating endothelial microparticles can be taken as a hallmark of stress-injured or dying endothelial cells and may be recognized in the future as a marker of endothelial dysfunction [8].