Skip to main content
Fig. 1 | Cardiovascular Diabetology

Fig. 1

From: Repressive H3K27me3 drives hyperglycemia-induced oxidative and inflammatory transcriptional programs in human endothelium

Fig. 1

High glucose triggers repressive H3K27me3 via derangement of histone-modifying enzymes. A Representative western blot images and relative densitometric quantifications showing H3K27me3 expression in HAEC exposed to normal (5 mmol/l) and high (25 mmol/l) glucose (n = 6/group). B Histone methyltransferases (EZH1, EZH2) and demethylases (UTX, JMJD3, UTY) mRNAs in the two experimental groups (n = 6/group) assessed by RT-qPCR. C Representative western blot images and densitometric quantifications of EZH2, UTX, and JMJD3 expression in HAEC exposed to normal and high glucose (n = 6/group). D, E Representative western blot images and densitometric quantifications showing H3K27me3 expression after reprogramming of chromatin-modifying enzymes (n = 6/group). F H3K27me3 protein expression in the presence of EZH2 selective inhibitor GSK126 (5 µmol/l) or vehicle alone (n = 6/group). G EZH2 gene expression assessed by RT-qPCR (n = 6/group) in HAEC exposed to the same experimental conditions. H Confocal microscopy images of H3K27me3 (green), EZH2 (red), and EZH2/H3K27me3 colocalization (yellow), and relative quantification of fluorescence intensity. Cell nuclei are stained with Hoechst (blue). Scale bar = 2 μm. (n = 12/group)

Back to article page