Figure 2.

Mbd2 Can Mediate RGC Apoptosis Caused by I/R Injury

RGCs were transfected with 50 nM Mbd2 siRNA or 1 μg/mL Mbd2 plasmid or scramble for 24 h and then left treated or untreated with ischemic stress for 2 h, followed by reperfusion for 2 h to induce apoptosis. (A and B) Representative flow cytometric data and cell apoptosis analysis results from four experimental groups showed that the knockdown of Mbd2 expression led to a significantly lower RGC apoptosis after I/R injury. (C–F) Western blot showed that Mbd2 siRNA significantly suppressed the expression of Mbd2 and cleaved caspase3. (G and H) Representative flow cytometric data and cell apoptosis analysis results indicated that the overexpression of Mbd2 can aggravate RGC apoptosis upon I/R. (I–L) The level of Mbd2 and cleaved caspase3 was significantly increased when RGCs were transfected with Mbd2 plasmid. Data were expressed as mean ± SEM of five independent experiments. #p < 0.05 versus the scramble group; *p < 0.05 versus the scramble/I/R group.