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Fig. 3 | Cardiovascular Diabetology

Fig. 3

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

Fig. 3

EZH2-mediated H3K27me3 signature contributes to NF-κB p65-dependent inflammatory changes. A, C Effect of NADPH oxidase inhibitor apocynin (100 µmol/l) and GSK126 (5 µmol/l) on high glucose-induced increase of NF-κB p65 binding activity (n = 3–6/group). B, D RT-qPCR showing gene expression of inflammatory markers (n = 6/group) in HAECs exposed to high glucose alone in the presence of apocynin (100 µmol/l), GSK126 (5 µmol/l), or vehicle alone. E Representative images and relative quantification of monocyte adhesion to HAEC exposed to high glucose in the presence and in the absence of TNFa (5 mmol/l) and treated with GSK126 (5 µmol/l) or vehicle alone (n = 3/group). Scale bar = 100 μm. IL-6 interleukin-6, TNFα tumor necrosis factor α, MCP-1 monocyte chemoattractant factor-1, ICAM-1 intercellular adhesion molecule 1, VCAM-1 vascular cell adhesion molecule 1

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