Full Length ArticleDownregulation of let-7e-5p contributes to endothelial progenitor cell dysfunction in deep vein thrombosis via targeting FASLG

- Differentially expressed let-7e-5p in EPCs from health control and DVT patients
- Let-7e-5p regulates migration and tube formation of EPC.
- FASLG is a validated target of let-7e-5p.
- Let-7e-5p and FASLG functionally regulate EPC function.
- Let-7e-5p increases EPC homing and CD34-positive vessels number.

This study aimed to evaluate the role of let-7e-5p in endothelial progenitor cells (EPCs) function and explore its therapeutic potential for deep vein thrombosis (DVT). We performed miRNAs screening and found that let-7e-5p was downregulated in DVT patients compared to control subjects. By using let-7e-5p agomir and antagomir, we demonstrated that let-7e-5p increased the migration and tube formation of human and rat EPCs. Based on bioinformatics, luciferase reporter assay and gene expression analysis, we identified Fas ligand (FASLG) as the target of let-7e-5p, and FASLG knockdown increased the migration and tube formation of EPCs. Furthermore, EPCs overexpressing let-7e-5p exhibited enhanced ability of homing and thrombus revascularization in rat model of venous thrombosis. In conclusion, let-7e-5p regulates the function of EPCs and is a potential therapeutic target in DVT treatment.