LncRNA GUSBP5-AS promotes EPC migration and angiogenesis and deep vein thrombosis resolution by regulating FGF2 and MMP2/9 through the miR-223-3p/FOXO1/Akt pathway.

Long non-coding RNAs (lncRNAs) play an essential role in multitudinous physiological and pathological processes, including vascular disease. We previously showed that lncRNA (enst00000511042) is upregulated in endothelial progenitor cells (EPCs) of deep veni thrombosis (DVT) patients. Here, we investigate the role and mechanism of in EPCs and DVT. Using the DVT model, we found that significantly reduced the thrombus size and weight and enhanced the homing ability of EPC to DVT sites to promote resolution and recanalization of thrombus. promoted cell cycle progression, proliferation, migration and invasion in EPCs, enhanced EPC angiogenesis and , and inhibited apoptosis. Strikingly, this study showed that was unbalanced and modulated Forkhead Box Protein O1 (FOXO1) in EPCs in patients with DVT by interacting with . Mechanistically, functions as a sponge of , which targets FOXO1. Both knockdown and overexpression remarkably inhibited angiogenesis, migration and invasion in EPCs. Additionally, our data suggested that activated the Akt pathway and enhanced fibroblast growth factor 2 (FGF2), matrix metalloproteinase-2/9 (MMP2/9) and F-actin expression. Taken together, this study indicates that modulates angiogenesis, proliferation and homing ability of EPCs via regulating FGF2 and MMP2/9 expression through the /FOXO1/Akt pathway, which may provide a new direction for the development of DVT therapeutics.