Modulation of monocyte-endothelial cell interactions by platelet microparticles.

Abstract

Platelets, activated by various agonists, produce microparticles (MP) from the plasma membrane, which are released into the extracellular space. Although the mechanism of MP formation has been clarified, their biological importance remains ill defined. We have recently shown that plateletderived MP influence platelet and endothelial cell function. In this study, we have further examined the mechanism of cellular activation by platelet MP. To address the possibility that they may influence monocyte-endothelial interactions, we used an in vitro assay to examine their effects on the ad-

Induction of apoptosis in circulating angiogenic cells by microparticles

“…Arachidonic acid is a major mediator of the cellular effects of microparticles (32,(37)(38)(39). We previously demonstrated that microparticles shuttle arachidonic acid from leukocytes to fibroblasts (30).…”

Cell‐derived microparticles in synovial fluid from inflamed arthritic joints support coagulation exclusively via a factor VII–dependent mechanism

“…P-selectin, which is present on platelet-derived microparticles, triggers monocytes to express not only tissue factor, but also chemokines (41,42). Platelet-derived microparticles transport arachidonic acid to endothelial cells and induce the expression of cyclooxygenase 2 and the increased production of prostacyclin (43), enhance the interaction between monocytes and endothelial cells (44), and enhance leukocyte aggregation and their accumulation on the endothelium (45). Furthermore, thrombin, factor Xa, and fibrin degradation products are all potent inducers of the inflammatory response (46)(47)(48)(49)(50).…”

Platelet Mediated Complement Activation

“…Compared to activated platelets, PMP can express 50-100 fold higher procoagulant activity (Sinauridze, Kireev, Popenko, Pichugin, Panteleev, Krymskaya, and Ataullakhanov 2007). They retain selected platelet membrane constituents, including glycoproteins Ib, IIbIIIa, and P-selectin (Gawaz, Ott, Reininger, Heinzmann, Neumann 1996;George, Pickett, Saucerman, McEver, Kunicki, Kieffer, and Newman 1986) which support vascular inflammation by participating in heterotypic communication with leukocytes and vascular endothelial cells (Martinez, Tesse, Zobairi, and Andriantsitohaina 2005;Barry, Pratico, Savani, and FitzGerald 1998).…”