EDIL3 knockdown inhibits retinal angiogenesis through the induction of cell cycle arrest in vitro

Pathological retinal angiogenesis is one of the most common causes of blindness, with limited treatment options being currently available. Epidermal growth factor (EGF)-like repeat and discoidin I-like domain-containing protein 3 (EDIL3) has been reported to serve an important role in embryonic vasculogenesis and tumor angiogenesis; however, its implication in retinal angiogenesis has yet to be elucidated. The present study aimed to investigate the putative roles of EDIL3 in retinal endothelial cells. RNA interference was used to disrupt the expression of EDIL3 in human retinal endothelial cells (HRECs) in vitro, and the resulting effects were examined. Cell proliferation was assessed using cell counting kit-8 reagent, Cell migration was investigated using a transwell chamber and a tube formation assay was used to study angiogenic capability in vitro. Flow cytometry was used to detect the cell cycle distribution and western blotting was used to study protein expression. The present results demonstrated that silencing EDIL3 expression significantly impaired the proliferative, migratory and tube forming capabilities of HRECs. Furthermore, EDIL3 knockdown was revealed to induce cell cycle arrest at the G(1) phase. Western blot analysis suggested that the possible mechanisms underlying the antiproliferative effects of EDIL3 silencing may involve the inhibition of EGF receptor-mediated pathways, and the suppression of cyclin D1 and cyclin E1 expression in HRECs. In conclusion, the findings of the present study suggested that EDIL3 may be implicated in retinal angiogenesis, and may have potential as a novel therapeutic target for the treatment of pathological angiogenesis.