Fig. 2

EZH2-mediated H3K27me3 signature contributes to oxidative stress. A Electron spin resonance (ESR) spectroscopy analysis of O₂⁻ production, B expression of ROS scavenging enzymes ALDH1, ALDH2, CAT, GPX1, SOD1 and SOD2 genes and C representative Western blots images and densitometric quantifications of SOD1 and SOD2 proteins in HAEC exposed to normal (5 mmol/l) and high (25 mmol/l) glucose treated with EZH2 inhibitor GSK126 (5 µmol/l) or vehicle alone (n = 6/group). D ChIP-qPCR assay showing the binding of H3K27me3 to SOD1 and SOD2 promoters in high glucose-treated cells and the inhibitory effect exterted by GSK126 (5 µmol/l; n = 3/group). E The interaction of H3K27me3 with JunD promoter in HAEC exposed to high glucose was also abolished by EZH2 inhibitor GSK126 as shown by ChIP-qPCR assay (n = 3/group), F–I Downregulation of JunD mRNA (n = 6/group), G JunD binding on NOX4 promoter (n = 3/group), and subsequent upregulation of H NOX4 gene and I protein expression (n = 6/group) in HAEC exposed to high glucose were blunted by GSK126 (5 µmol/l) but not DMSO vehicle alone. IgG controls of ChIP-qPCR assay are also shown