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Mbd2 mediates retinal cell apoptosis by targeting the lncRNA Mbd2-AL1/miR-188-3p/Traf3 axis in ischemia/reperfusion injury
Molecular Therapy - Nucleic Acids ( IF 5.919 ) Pub Date : 2020-01-18 , DOI: 10.1016/j.omtn.2020.01.011
Yanni Ge; Ran Zhang; Yuqing Feng; Huiling Li

Recent studies reported that DNA methylation was involved in retinal cell death. Methyl-CpG binding domain protein 2 (Mbd2) is one of DNA methylation readers. Its role and mechanism of regulation remain unclear. The ischemia/reperfusion (I/R) model in mice primary culture retinal ganglion cells and Mbd2 knock-out (Mbd2-KO) mice were used in the current study. We demonstrated that Mbd2 mediates RGCs apoptosis caused by I/R injury. Mechanistically, the data suggested that Mbd2 upregulated Mbd2-associated long non-coding RNA 1 (Mbd2-AL1) via demethylation of its promoter. Furthermore, Mbd2-AL1 sponged miR-188-3p, thus preventing TNF receptor associated factor 3 (Traf3) downregulation and inducing RGCs apoptosis. This was further demonstrated by the fact that inhibition of miR-188-3p diminished the anti-apoptosis role of Mbd2-AL1 siRNA. Finally, it showed that the apoptosis of retinal cells was attenuated and the visual function was preserved in Mbd2-KO mice which was associated with the Mbd2-AL1/miR-188-3p/Traf3 axis. Our present study revealed the role of Mbd2 in RGCs apoptosis which may provide a novel therapeutic strategy for retinal ischemic diseases.
更新日期:2020-01-21

 

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