Background:The mechanisms of pathological retinal neovascularization (RNV) remain unknown.Several microRNAs were reported to be involved in the process of RNV.Oxygen-induced retinopathy (OIR) is a useful model to investigate RNV.Our present work explored the expression and the role of microRNA-128 (miR-218) in oxygen-induced RNV.Methods:OIR was used to establish RNV model.The expression level ofmiR-218 in the retina from OIR mice was assessed by quantitative real-time reverse transcfiptase polymerase chain reaction.Fluorescein angiography was performed in retinae of OIR mice,and RNV was quantified by hematoxylin and eosin staining to evaluate the effect of pCDH-CMV-miR-218 intravitreal injection on RNV in OIR mice.Roundabout 1 (Robo 1) expression was detected by West blotting in mouse retinal vascular endothelial cells expressing a high or low level ofmiR-218 and retinal tissues from OIR mice.Cell migration was evaluated by scratch wound assay.Results:In OIR mice,the expression level of miR-218 was significantly down-regulated (P =0.006).Retinal Robo1 expression was significantly increased at both mRNA and protein levels (P =0.001,0.008;respectively),miR-218 intravitreal injection inhibited retinal angiogenesis in OIR mice,and the restoration of miR-218 in retina led to down-regulation of Robo 1.Conclusions:Our experiments showed that restoration of miR-218 inhibited retinal angiogenesis via targeting Robo 1.MiR-218 contributed to the inhibition of retinal angiogenesis and miR-218 might be a new therapeutic target for preventing RNV.