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. Author manuscript; available in PMC: 2022 Sep 1.
Published in final edited form as: Bone. 2021 Apr 30;150:115993. doi: 10.1016/j.bone.2021.115993

Figure 5: Optimal Ezh2 inhibition modulates levels of H3K27me3 and H3K27ac marks.

Figure 5:

MC3T3 cells were treated with vehicle (Vehicle 1 = 0.05% DMSO or Vehicle 2 = 0.4% DMSO) or optimal doses of each compound (40μM for CPI-169 and 5μM for all other compounds) for the first six days of osteogenic differentiation. (A) Western blot of Ezh2 protein, H3K27me3 and H3K27ac relative to H3, Gapdh and Tubulin three days after initial treatment with each of the Ezh2 inhibitors (Vehicle 1A and 1B are both at 0.05% DMSO). (B) Diagram showing interrelationships between H3K27me3 and H3K27ac levels that are controlled as indicated by Ezh2, lysine demethylases (KDMs), histone acetyl transferases (HATs), as well as histone deacetylases (HDACs) and their cognate inhibitors (iHDACs). The western blot data in panel A are consistent with a shift from left to right to decreased total H3K27me3 levels concomitant with an increase in total H3K27ac levels that together support osteoblast differentiation.