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. Author manuscript; available in PMC: 2019 Jun 21.
Published in final edited form as: Free Radic Biol Med. 2019 Feb 18;134:630–643. doi: 10.1016/j.freeradbiomed.2019.02.015

Fig. 4. An induction of H3K9Me2 attenuated the transcriptional activity of Nrf2 and reduced the antioxidant levels.

Fig. 4

(A) The quantitative RT-PCR analysis data shows that TBI causes a decrease in the mRNA level of sod and catalase both in the retina and optic nerve compared to sham mice. (B) Western blot analysis data suggests that TBI leads to a decrease in the expression level of SOD and Catalase in both retina and optic nerve compared to sham mice. (C) The expression level of Nrf2 in nucleus show that there is no difference either in the retina or optic nerve following TBI compared to sham. (D) The chromatin immunoprecipitation (ChIP) data shows that the binding of Nrf2 to the sod promoter was decreased in the retina and optic nerve after TBI compared to sham mice. (E) Western blot analysis show that the level of H3K9Me2 and G9a was increased in the retina and optic nerve after TBI compared to sham mice. (F) Confocal microscopic analysis shows that TBI leads to an increase in the expression level of G9a and H3K9Me2 in RGC after TBI. (G) Confocal microscopic data shows that TBI leads to an increase in G9a and H3K9Me2 in the optic nerve following TBI. (H) The co-immunoprecipitation (IP) analysis show that the interaction between Nrf2 and H3K9Me2 was increased significantly in both retina and optic nerve following TBI. Statistical significance was measured by one-way ANOVA with a Tukey-Kramer post-hoc correction, n = 5, *p < 0.05. All data are expressed as mean ± S.E.M.