Fig. 4: EHMT2 promotes VSMC proliferation in a methyltransferase activity-dependent manner.
From: EHMT2 aggravates vascular remodeling via epigenetic inhibition of GADD45G
a Analysis of histone methyltransferase sequence alignment across different species, with a specific focus on the rat p.Ala1130 residue and other residues linked to enhanced functional activity. b Structure of EHMT2 SET domain dimers interacting with histone H3 and SAM. Magnification revealing that the formation of hydrogen bonds between residue p.Ala1130 in EHMT2 and the histone tail residue and other EHMT2 residues. c Representative western blot analysis and quantification of H3K9me2, SM22α and PCNA expression in oe-EHMT2, oe-EHMT2(A1130S) and control lentivirus vector-transfected VSMCs (n = 4). d VSMC (n = 4) proliferation was assessed via a Ki-67 assay, and nuclei were stained with DAPI. Scale bar, 100 μm. e Representative images of wound-healing assays. Images were taken at 0 and 12 h after scratching monolayers of oe-EHMT2 VSMCs, oe-EHMT2 (A1130S) VSMCs and control VSMCs (n = 3). f Representative images and quantitative analysis of the migration of VSMCs (n = 5) treated with oe-EHMT2 and oe-EHMT2 (A1130S). Scale bar, 400 µm. The data are presented as mean ± s.e.m. P values were calculated using an unpaired two-tailed t-test (d–f) or a two-way ANOVA (c).
