Objective To explore the role of the base mismatch repair gene Mutyh in retinopathy of prematurity(ROP).Methods Mutyh(-/-)and wild-type(WT)mice were used for the modeling of oxy-gen-induced retinopathy.The retinal oxidative stress was examined,and the ultrastructures of photoreceptors and mitochondria were observed.The biomarkers of photoreceptors and mitochondria were tested.Furthermore,the photoreceptor cell line 661W was treated with hydrogen peroxide for the modeling of oxidative stress.In the cell model,and the oxidative stress and photoreceptor functions in the cells were measured.Results In both the mouse and cell models,the expression of Mutyh was up-regulated.Mutyh knockout in mice and knockdown in cells exerted negative effects on photoreceptors and mitochondria.Mutyh overexpression showed protective func-tions in the cell model,indicating that Mutyh played a role in repairing photoreceptors and mitochondria.Conclusions Mutyh showed the potential to become a biomarker of ROP.Increasing Mutyh expression might have therapeutic effects on ROP,which needs further validation.
关键词
早产儿视网膜病变/氧化应激/氧诱导的视网膜病变/感光细胞/Mutyh
Key words
retinopathy of prematurity/oxidative stress/oxygen-induced retinopathy/photoreceptor/Mutyh
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