Extracellular vesicles (EVs) released from various cell types can mediate paracrine signalling and control important pathophysiological responses. MicroRNAs transferred within EVs represent one of the main mechanisms by which they influence the recipient cells. Circulating endothelial progenitor cells (EPCs) release EVs that are readily taken up by endothelial cells. We hypothesized that EPC derived EVs can be manipulated to deliver specific microRNAs to endothelial cells and thereby modulate their angiogenic response. Human EPCs isolated from the umbilical cord blood displayed endothelial imunophenotype, being positive for CD31, CD146 and CD105 and negative for haemathopoetic markers CD45 and CD14. EVs were collected by ultracentrifugation of the EPC conditioned media. To identify microRNAs exported from EPCs, the small RNA contents of EPCs and their EVs were analyzed by deep sequencing. Several miRNAs were highly enriched in EVs compared to their expression levels in EPCs and there was remarkable consistency in miRNA expression in the cultures from different donors. EVs were then isolated from EPCs transfected with several vectors driving the expression of microRNAs, including miR-146a, and miR-451. Enrichment of these microRNAs in EPC EVs was demonstrated by RT-qPCR. Following direct transfection of human microvascular endothelilal cells (HMEC) with plasmid vectors driving the expression of miR-146a, downregulation of specific miR-146a predicted target genes such as CCND2, ELAVL1 and CRIM1, was revealed by microarray. When HMECs were incubated with miR-146a enriched EPC derived EVs, these EVs were taken up by HMECs, resulting in the reduced mRNA expression of the same miR-146a targets. We show that the content of EPC released EVs can be manipulated to include significant amounts of exogenous miRNAs, which can be taken up by endothelial cells. The ability of EVs to carry anti- or pro-angiogenic microRNAs can be exploited to modulate angiogenesis in various models and may have therapeutic applications in multiple disease conditions associated with abnormal angiogenesis.