MiR-150 promotes angiogensis and proliferation of endothelial progenitor cells in deep venous thrombosis by targeting SRCIN1.

Venous thromboembolism (VTE), encompassing deep venous thrombosis (DVT) and pulmonary embolism (PE), is the third most common cardiovascular disease. miR-150 is one of important microRNAs which play critical role in various cellular function such as endothelial progenitor cells (EPCs). In this study, we investigate the effect of miR-150 on EPCs function ex vivo and thrombus resolution in vivo. We determined miR-150 expression in EPCs isolated from DVT patients and control subjects by RT-PCR. Potential target of miR-150 was confirmed by bioinformatics analysis and luciferase reporter respectively. The angiogenesis and proliferation were tested by MTT and tube formation assay. A murine model of venous thrombosis was developed as in vivo model. Finally, the effect of miR-150 on EPCs with inferior venous thrombosis were evaluated in vivo. Our data showed that miR-150 was downregulated in EPCs from DVT patients. By using miR-150 agomir and antagomir, we found that miR-150 promoted angiogenesis and proliferation of EPCs. Bioinformatics analysis revealed SRCIN1 as a target of miR-150 and SRCIN1 knockdown inhibited function of EPCs. Forced expression of miR-150 contributed thrombus resolution in a murine model of venous thrombosis. In general, miR-150 was downregulated in EPCs from DVT. Upregulation of miR-150 promoted angiogenesis and proliferation of EPCs by targeting SRCIN1 in vitro and thrombus resolution in vivo.