MiR-497-5p Ameliorates Deep Venous Thrombosis by Facilitating Endothelial Progenitor Cell Migration and Angiogenesis by Regulating LITAF.

Deep vein thrombosis (DVT) is a clinical manifestation of venous thromboembolism and a major global burden of cardiovascular disease. In recent years, the crucial role of microRNAs (miRNAs) in cardiovascular disease has been confirmed. Here, we aimed to investigate the specific effect of miR-497-5p on DVT. The endothelial progenitor cells (EPCs) were obtained from the bone marrow of newborn rats and transfected with miR-497-5p mimics or/and pcDNA3.1/lipopolysaccharide-induced TNF factor (LITAF). The proliferation and migration abilities of EPCs were detected using CCK-8 assay and transwell assay, respectively. Angiogenesis was evaluated using tube formation assay. The interaction of miR-497-5p and LITAF was confirmed by luciferase reporter experiment. DVT rat model in vivo was established by inferior vena cava (IVC) ligation in Sprague-Dawley rats. Histological analysis of IVC tissue was conducted by hematoxylin-eosin staining. We found that enhancing miR-497-5p expression facilitated the abilities of proliferation and migration of EPCs. Additionally, overexpression of miR-497-5p increased the capacity of EPCs to form capillary tubes on Matrigel. LITAF was found to be targeted by miR-497-5p and negatively regulated by miR-497-5p. Overexpression of LITAF counteracted the miR-497-5p overexpression's effect on the proliferation, migration, and angiogenesis abilities of EPCs. Moreover, the injection of agomir-miR-497-5p alleviated thrombus formation, reduced thrombus weight, and reduced the serum level of D-dimer in DVT rat model by reducing LITAF expression. This study suggests that miR-497-5p alleviates DVT by facilitating EPCs proliferation, migration, and angiogenesis by targeting LITAF.