Fig. 5

EGR2 deficiency mitigates the hypoxia-induced inflammatory response and apoptosis in cardiomyocytes. A Western blot analysis of the relative EGR2 protein expression level in WT and EGR2 knockout cardiomyocytes, GAPDH was served as internal control; B the inflammation related genes expression in hypoxia-induced WT and EGR2-KO cardiomyocytes detected by qPCR assays. GAPDH was served as internal control, n = 3 in each group; C qPCR analysis of the genes expression related to apoptosis in hypoxia-induced WT and EGR2-KO cardiomyocytes. GAPDH was used as internal control, n = 3 in each group; D representative Western blot images of BAX and BCL2 expression in hypoxia-induced WT and EGR2-KO cardiomyocytes. GAPDH was used as internal control, n = 3 in each group. *p < 0.05, **p < 0.01; All data are shown as the mean ± SD. Abbreviations: WT wild type, KO knockout, IL-6 interleukin 6, IL-1b interleukin 1b, CCL2 C–C motif chemokine ligand 2, TNF tumor necrosis factor, BAX BCL2 associated X, BAD BCL2 associated agonist of cell death, BCL2 B cell lymphoma protein-2