Figure 10.
Knockout of Mbd2 Promotes RGC Survival in I/R injury
The intraocular pressure (IOP) of homozygous mice deficient in Mbd2 and wild-type littermates was elevated to 120 mmHg for 1 h, and the retinas were then dissected at indicated time points. (A and B) Effect of Mbd2 deletion on RGC survival in vivo. Representative images of retinal flat-mount immunostaining for Tuj1 to visualize surviving ganglion cells in mice at 7 days after induction of I/R or the sham group, with or without deletion of Mbd2. Original scale bars, 50 μm. Mean count of RGCs normalized to the Mbd2-WT/sham group. (C and D) Representative sections of TUNEL-positive cells in retina at 24 h after induction of I/R or the sham group, with or without deletion of Mbd2. Original scale bar, 100 μm. Mean number of TUNEL-positive RGCs normalized to total nuclei in the ganglion cell layer. Four central retina slices were analyzed per animal. (E and F) Representative scotopic ERG traces in Mbd2-WT and Mbd2-KO mice, with or without I/R, at an intensity of 3.0 cds/m2 at 2 and 7 days postretinal ischemia. Comparison and statistical analysis of b-wave amplitudes among four groups at 3.0 cds/m2 scotopic ERG. The data were expressed as mean ± SEM of five independent experiments. #p < 0.05 versus the Mbd2-WT/sham group; *p < 0.05 versus the Mbd2-WT/I/R group.