Fig. 3
From: Super enhancers targeting ZBTB16 in osteogenesis protect against osteoporosis

SE disorder of MSCs leads to the OP phenotype and delayed bone repair. a DNA electrophoresis was performed to genotype genetically modified mice. b Immunoblot analysis of BRD4 protein expression in different organs of the Brd4fl/fl and Brd4fl/fl Prx1-cre mice. Scatter plot showing the relative protein abundance of BRD4. c Micro-CT analysis of the Brd4fl/fl and Brd4fl/fl Prx1-cre mice, and the trabecular bones were 3D reconstructed. Bone morphometric analysis was performed, and the parameters included bone BV/TV, Tb. Th, Tb. N, Tb. Sp and cortical Ct. Th. d HE and Masson staining of femurs from the Brd4fl/fl and Brd4fl/fl Prx1-cre mice. Scatter plot showing the quantification of Masson staining. e ARS and ALP staining of osteogenic differentiating MSCs extracted from the Brd4fl/fl and Brd4fl/fl Prx1-cre mice. Quantification of ARS and ALP are shown in the scatter plots. f Diagram showing the workflow of calvarial and femoral defect induction and analysis. g Micro-CT analysis showing the calvarial and femoral defects of the Brd4fl/fl and Brd4fl/fl Prx1-cre mice. h CUT&Tag profile heatmap of BRD4 in MSCs from the Brd4fl/fl and Brd4fl/fl Prx1-cre mice. The statistical data are represented as the means ± SEMs, n = 9 (n = 5 in c), *P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.001