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

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.
Source: Microvascular Research - Category: Biochemistry Source Type: research