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

Figure 7.

Figure 7

Effects of JQ-1 and methylprednisolone treatment on Foxp1 signaling, bone histology, and ex vivo osteogenesis and adipogenesis. JQ-1 treatment attenuated glucocorticoid-mediated upregulation of BRD4 and Foxp1 levels and improved H3K9ac levels (a). Glucocorticoid-induced loss of trabecular bone histology (scale bar, 120 μm) (b) and fluorescent calcein-labeled mineral acquisition (scale bar, 30 μm) (c), and marrow adiposity (Upper scale bar, 25 μm; lower scale bar, 8 μm) (d,e) were improved in the GC + JQ-1 group. JQ-1 treatment mitigated glucocorticoid-augmented adipocyte formation (scale bar, 8 μm) (f) and improved mineralized matrix formation (scale bar, 10 μm) (g) of primary bone-marrow mesenchymal cells. Trabecular histology, mineralization and adipocyte formation of bone-marrow stromal cells were probed using von Kossa staining, calcein labeling, and Oil Red O staining, respectively. Data are expressed as mean ± SEM calculated from 6 mice. Asterisks * indicate significant differences from the vehicle group and hashtag # indicates significant differences from the GC group (p < 0.05). GC: glucocorticoid; Veh: vehicle.