Journal: Cardiovascular Diabetology
Article Title: Repressive H3K27me3 drives hyperglycemia-induced oxidative and inflammatory transcriptional programs in human endothelium
doi: 10.1186/s12933-024-02196-0
Figure Lengend Snippet: Targeting EZH2-H3K27me3 epigenetic signature rescues abnormal phenotypes in endothelial cells isolated from patients with diabetes. A Representative confocal microscopy images of H3K27me3 (green), EZH2 (red), and EZH2/H3K27me3 colocalization (yellow) and densitometric quantification of fluorescence intensity. Cell nuclei are stained with Hoechst (blue). Scale bar = 2 μm. n = 6/group. B and C RT-qPCR arrays showing gene expression of SOD1 , SOD2 , JunD , and C NOX4 , respectively (n = 3/group). D electron spin resonance (ESR) spectroscopy analysis of O 2 − production (n = 3/group). E NF-κB p65 binding activity (n = 6/group), and F gene expression of IL-6 and MCP-1 (n = 3/group). IL-6, interleukin-6; MCP-1, monocyte chemoattractant factor-1
Article Snippet: NF-κB p65 binding activity in HAEC and D-HAEC was measured by the TransAMTM NF-κB p65 activation protein assay kit (Active Motif; Carlsbad, CA, USA), following the manufacturer’s instructions.
Techniques: Isolation, Confocal Microscopy, Fluorescence, Staining, Quantitative RT-PCR, Gene Expression, Electron Paramagnetic Resonance, Spectroscopy, Binding Assay, Activity Assay