Figure 5.

lncRNA Mbd2-AL1 Mediates RGC Apoptosis upon I/R Injury

RGCs were transfected with 50 nM Mbd2-AL1 siRNA or 1 μg/mL Mbd2-AL1 plasmid or scramble, 24 h before I/R and following I/R for 2/2 h. (A and B) Representative flow cytometry data and statistical analysis results of cell apoptosis from four experimental groups showing that the deletion of Mbd2-AL1 attenuated I/R-induced RGC apoptosis. (C) The levels of Mbd2-AL1, with or without I/R treatment, were analyzed by quantitative real-time PCR. The level of Mbd2-AL1 was increased after I/R interference. Mbd2-AL1 siRNA suppressed the expression of Mbd2-AL1 in both scramble and I/R group. (D–F) Western blot results showing the expression of cleaved caspase3 and caspase3 with statistical data analysis. β-Tubulin was used as internal control. Mbd2-AL1 siRNA could suppress the expression of cleaved caspase3 induced by I/R injury. (G and H) Representative flow cytometric data and statistical analysis results of cell apoptosis from four experimental groups showed that the overexpression of Mbd2-AL1 aggravated I/R-induced apoptosis. (I) Quantitative real-time PCR showing the levels of Mbd2-AL1, with or without I/R treatment. The level of Mbd2-AL1 was increased after I/R injury. Transfection of exogenous Mbd2-AL1 plasmid significantly increased the expression level of Mbd2-AL1 in both scramble and I/R group. (J–L) Western blot showing the expression of cleaved caspase3 and caspase3 with statistical data analysis. Transfection of exogenous Mbd2-AL1 plasmid increased the expression of cleaved caspase3 in both scramble and I/R group. β-Tubulin was used as internal control. The 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.