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Slit-miR-218-Robo axis regulates retinal neovascularization.
Int J Mol Med. 2016 Apr;37(4):1139-45. doi: 10.3892/ijmm.2016.2511. Epub 2016 Feb 29.
Kong Y1, Sun B2, Han Q1, Han S1, Wang Y1, Chen Y1.
1Tianjin Eye Hospital, Heping, Tianjin 300020, P.R. China.
2Key Laboratory of Hormones and Development, Ministry of Health, Heping, Tianjin 300070, P.R. China.
Abstract
miR-218 is an important intronic microRNA (miRNA or miR) which is known to regulate angiogenesis in tumors. The present study aimed to investigate the effects of miR-218, as well as its host genes, Slit2 and Slit3, on oxygen-induced retinal neovascularization (RNV) and to explore the associated mechanisms of action. For this purpose, a mouse model of oxygen-induced retinopathy (OIR) was established. The expression levels of miR-218-1 and miR-218-2, as well as those of their host genes, Slit2 and Slit3, were determined by RT-qPCR. Fluorescein angiography was performed on the retinas of the mice with OIR, and RNV was quantified by H&E staining in order to evaluate the effect of pCDH-CMV-miR-218 intravitreal injection on RNV in the mouse model of OIR. Roundabout, axon guidance receptor, homolog 1 (Robo1) expression was detected in mouse retinal vascular endothelial cells expressing high or low levels of miR-218 and in retinal tissues from mice with OIR by western blot analysis. Cell migration was evaluated by a scratch wound assay. We noted that in the mice with OIR, the expression level of miR-218 was significantly downregulated. We also noted that Robo1 expression was suppressed by miR-218. Furthermore, in the mice with OIR, the expression level of miR-218 was significantly downregulated, and that of miR-218-1 and its host gene, Slit2, was concomitantly downregulated as well. The restoration of miR-218 inhibited retinal angiogenesis by targeting Robo1. Taken together, our findings suggest that the Slit2-miR-218-Robo1 axis contributes to the inhibition of retinal angiogenesis and that miR-218 may be a new therapeutic target for preventing RNV.
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