On the Trail of Microparticles

Abstract

Stimulation of a variety of cell types leads to the release of submicron vesicles that bud off from the plasma membrane. These so-called microparticles (MPs) or microvesicles are defined by their small size (0.1 to 1 μm) and the presence of surface antigens from the parental cells.1,2 MPs contribute to a variety of physiological and pathological processes. For instance, they appear to play a role in both hemostasis and thrombosis. MPs released into the bloodstream can act as messengers delivering a variety of cargos, such as cell surface receptors, proinflammatory cytokines, signaling molecules, and even mRNA, to distal cells.1,2 They may also contribute to disease by transporting viruses and prions.1,2 In addition, in vitro studies have shown that binding of MPs to endothelial cells and monocytes induces the expression of proinflammatory and procoagulant molecules (Figure 1). In this issue of Circulation Research , Simoncini et al explore the inflammatory pathways that trigger the release of MPs from endothelial cells.3 Figure 1. MPs derived from different cell types induce the expression of proinflammatory and procoagulant molecules in endothelial cells, monocytes, and epithelial cells. Monocyte-derived MPs also bind to activated platelets. MPs derived from endothelial precursor cells (EPC) bind to endothelial cells and enhance angiogenesis. TF indicates tissue factor. MPs are generated from a variety of different vascular cell types, including endothelial cells, monocytes, and platelets. Early studies on MPs focused on platelets because these cells readily generated MPs on activation. Indeed, the original term for MPs was “platelet dust” and platelets are the major source of MPs in the blood of healthy individuals.4 Importantly, the procoagulant activity of MPs can be significantly increased by altering the phospholipid composition of the membrane surface. Under normal conditions the distribution of phospholipids moieties in the plasma membrane of …