Transplantion of bone marrow-derived endothelial progenitor cells (EPCs) may be a novel treatment for deep venous thrombosis (DVT). This study probed into the role of miR-361-5p in EPCs and DVT recanalization. EPCs were isolated from male SD rats and identified using flow cytometry. The viability, migration and tube formation of EPCs were examined using MTT assay, wound-healing assay and tube formation assay, respectively. Target gene and potential binding sites between miR-361-5p and FGF1 were predicted by starBase and confirmed by dual-luciferase reporter assay. Relative expressions of miR-361-5p and FGF1 were detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. A DVT model in SD rats was established to investigate the role of EPC with miR-361-5p antagomir in DVT by hematoxylin-eosin staining. EPC was identified as 87.1% positive for CD31, 2.17% positive for CD133, 85.6% positive for vWF and 94.8% positive for VEGFR2. MiR-361-5p antagomir promoted proliferation, migration and tube formation of EPCs and upregulated FGF1 expression, thereby dissolving thrombus in the vein of DVT rats. FGF1 was the target of miR-361-5p, and overexpressed FGF1 reversed the effects of upregulating miR-361-5p on suppressing EPCs. Downregulation of miR-361-5p enhanced thrombus resolution in vivo and promoted EPC viability, migration and angiogenesis in vitro through targeting FGF1. Therefore, miR-361-5p may be a potential therapeutic target for DVT recanalization.

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