Fig. 1
From: Nup133 and ERα mediate the differential effects of hyperoxia-induced damage in male and female OPCs
Hyperoxia leads to impairment of maturation and an overall severe effect on the male OPCs. a Western blot analysis of male and female OPCs with anti-CNPase antibody at normal (3% O2) differentiation conditions and 24 h post 80% O2 shock, showing a significant decrease in expression in the male OPCs. In all the figures, M_N represents male normoxia, M_H male hyperoxia, F_N female normoxia, and F_H female hyperoxia. b Representative images of male and female OPCs stained for the OPC maturation marker CNPase after differentiation under normal oxygen conditions and post 24 h 80% O2 shock. Scale bar represents 75 μm. Data are representative of three independent experiments. Bars and error represent mean ± SEM of replicate measurements. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (Student’s t test). c Venn diagram of significantly altered proteins (normalized to the normoxic conditions) in male and female OPCs post 24 h 80% O2 treatment. Cutoff p value < 0.05. d Functional categorization of significantly enriched proteins in male OPCs and female OPCs post 24 h 80% O2 treatment using Ingenuity Pathway Analysis (IPA) software. Bar graphs depict the most extensively enriched biological processes among the altered proteins. Cutoff p value < 0.05 (Fisher’s exact test). e Heat map representation of mitochondrial and stress response proteins that were dysregulated in male- and female-derived OPCs post 24 h 80% O2 treatment in comparison to 3% O2 (normoxia) controls. Highly downregulated proteins are indicated in red, intermediate in yellow, and highly upregulated proteins in green. Proteins are sorted according to IPA categories. Cells marked with *represents the significantly altered proteins in each group. The cutoff p value < 0.07. Data are representative of five independent experiments