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. 2020 Jun 19;9(6):1500. doi: 10.3390/cells9061500

Figure 1.

Figure 1

Analyses of H3K9ac action to glucocorticoid modulation of osteogenesis and adipogenesis of bone-marrow mesenchymal stem cells. Glucocorticoid increased Hdac4 levels, but reduced H3K9ac signaling (a). Hdac4 interference increased H3K9ac levels (b), attenuating glucocorticoid-induced repression of mineralized matrix formation (scale bar, 5 mm) (c), osteocalcin and Runx2 expression (d), as well as reversed H3K9ac enrichment in Runx2 promoter (e). Hdac4 knockdown alleviated glucocorticoid-mediated adipocyte formation (scale bar, 8 μm) (f) and PPARγ2 expression (g). Loss of Hdac4 function did not significantly change H3K9ac occupancy in the PPARγ2 promoter (h). Forced HDAC4 expression decreased H3K9ac levels, binding the Runx2 promoter and osteogenic differentiation, whereas adipocyte formation was increased. Mineralized matrix, adipocyte, mRNA expression, and H3K9ac enrichment in the promoter were probed using von Kossa staining, Nile Red fluorescence staining, qRT-PCR, and ChIP-PCR, respectively. Data are expressed as mean ± SEM calculated from 3 experiments. Asterisks * indicate significant differences from the scramble group, hashtag # indicates significant differences from the GC group (p < 0.05), and @ indicates significant differences from the vector group. GC: glucocorticoid; Veh: vehicle.