Figure 1.

I/R Induced the Expression of Mbd2 in Mice RGCs and Retinas

(A and B) Cultured primary mouse RGCs were treated with or without Ca²⁺ (2 μM) and antimycin (10 μM) in HBSS (ATP and glucose depletion) at indicated time periods (ischemia/reperfusion for 0/0 h, 2/0 h, 2/2 h, and 2/4 h, respectively). Mbd2 levels were analyzed by western blotting. I/R induces an increase of Mbd2 levels in mice RGCs. The data are shown as mean ± SEM of five independent experiments. #p < 0.05 versus the 0/0 group. (C and D) The intraocular pressure was elevated to 120 mmHg for 1 h to induce a transient retinal ischemia and then exposed to reperfusion for 6 h, 12 h, and 24 h in C57BL/6 mice, respectively. The level of Mbd2 expression gradually increased in the retinas following ischemic reperfusion injury. Immunoblot signals were quantified by densitometry and normalized to the internal control β-tubulin. The data are shown as mean ± SEM of five independent experiments. #p < 0.05 versus the 0/0 group. (E and F) Immunofluorescent staining of retinal sections from 24-h reperfusion and after 1 h ischemia compared with control animals. The green signal represents the subcellular localization of Mbd2 in nucleus. The number of Mbd2-positive cells in the RGC layer was significantly higher than in the sham group (yellow arrowheads). The data are shown as mean ± SEM of five independent experiments. #p < 0.05 versus the sham group.