Plasma membrane blebbing results in the formation of microparticles (MP) that may vary in size from 100 to 1000 nm. MPs contain chemokines, receptors, lipids as well as an mRNA and an miRNA pool. Quantitative differences in the miRNA content of vesicles in response to different release of stimuli suggest that the vesicle formation is an active process. Platelets are a major source of MPs in the circulation. Several lines of evidence highlight an important role for platelet MPs in cardiovascular diseases. These microvesicles carry miRNAs that can have a paracrine effect and modulate vascular endothelial cell function. For example, Laffont et al. (2013) demonstrated a transfer of platelet MP-derived Ago2/miR-223 complexes to endothelial cells. These complexes were functional and could regulate gene expression in the recipient cells as demonstrated by the altered expression of endogenous targets at the mRNA and protein level. In response to advanced glycation end products, platelet MPs were also shown to promote endothelial cell apoptosis by delivering miR-223 into endothelial cells and inhibiting protein expression of the endogenous IGF-1 receptor (Pan et al. 2014). On a different note, the miR-223 transfer to naive monocytes via macrophage-derived MPs can induce differentiation to macrophages, while silencing miR-223 impaired survival in monocytes (Ismail et al. 2013). Besides platelets, endothelial MPs were shown to limit apoptosis and enhance vascular repair by delivering miR-126 to recipient cells. Increased miR-126 levels inhibited sprouty-related, EVH1 domain-containing protein 1 (SPRED1) and led to an increase in reendothelialization in vitro. Under hyperglycemic conditions, lower expression of miR-126 was observed, and this protective effect was largely abolished. Interestingly, miR-126 levels in circulating MPs were reduced in diabetic patients (Jansen et al. 2013). MPs also seem to mediate the intercellular communication between monocytes and endothelial cells in the angiogenic process. The miR-150 content of monocytic MPs was reported to promote angiogenesis in vitro and in vivo, although the mechanisms involved are still not well understood (Li et al. 2013; Zhang et al. 2010).

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