Fig. 1

H3K36me3 was negatively correlated with HASMC proliferation and neointima formation. A-B. Western blot analysis showed the protein expression of H3K36me1, H3K36me2, and H3K36me3 in HASMCs cultivated with 0.5%, 2%, and 10% fetal bovine serum (FBS) (n = 4 per group). β-Actin served as a loading control. *P < 0.05, **P < 0.01. C. Representative images of H&E staining of carotid arteries in the control group and vascular injury (VI) group. Scale bar: 20 and 50 μm. D. Representative images of immunohistochemical staining of H3K36me3 in the carotid arteries. H3K36me3-labeled nuclei are shown in brown. Scale bar: 20 and 50 μm. E. Cell viability of HASMCs after treatment with different concentrations of JIB-04 (0, 0.1, 0.25, 0.5, 1, 2.5, 5, and 10 μM) (n = 5 per group). F. The toxicity of different concentrations of JIB-04 (0, 0.1, 0.25, 0.5, 1, 2.5, 5, and 10 μM) on HASMCs was evaluated by LDH release levels (n = 5 per group). G-H. H3K36me1, H3K36me2, and H3K36me3 protein levels in HAMSCs treated with different concentrations of JIB-04 (0, 0.1, 0.25, 0.5, and 1 μM) were measured by western blotting (n = 4 per group). β-Actin served as a loading control. *P < 0.05, **P < 0.01, N.S. no significant