Fig. 5: A sheet of rBMSCs with FOXA2 knockdown accelerated bone fracture healing in a rat tibial defect model. | Cell Death & Disease

Fig. 5: A sheet of rBMSCs with FOXA2 knockdown accelerated bone fracture healing in a rat tibial defect model.

From: Knockdown of FOXA2 enhances the osteogenic differentiation of bone marrow-derived mesenchymal stem cells partly via activation of the ERK signalling pathway

Fig. 5

a The results of biomechanical analysis indicated that treatment with rBMSCs with FOXA2 knockdown markedly increased the ultimate force and stiffness when compared with the blank group and KD-NC group. b Radiographic analysis taken at 8 weeks postoperatively. c Quatitive μCT analyses of BV/TV and Tb.N. d 3D construction images of μCT analyses. d Histological evaluation including HE, Safranin O and fast green, and Masson staining of the defect area at 8 weeks after surgery in each group showed that the defects in the blank group were filled with fibrous tissue and a few chondrocytes without bridging bone formation, while a thick callus consisting of newly formed woven bone tissue was observed in the defect area in the KD-NC group. In the FOXA2 knocked down rBMSC group, the defect sites were almost sealed, and remodelling of the callus was more complete. Yellow arrow: the defect area. Scale bars, 500 μm. Data are expressed as the mean ± SD. *P < 0.05 vs. blank group; #P < 0.05 vs. KD-NC. KD knockdown of FOXA2, KD-NC negative control of FOXA2 knockdown

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