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. 2021 Mar 4;12(3):238. doi: 10.1038/s41419-021-03517-x

Fig. 6. hBMSCs with AAV2-USP53 improved bone formation in vivo.

Fig. 6

a Experimental design of the mouse calvarial defect model. b Critical-size calvarial defects (5 mm in diameter) in mice were treated with AAV2-control-infected hBMSCs or AAV2-USP53-infected hBMSCs in fibrin matrix with PBS. Eight weeks after surgery, bone regeneration was measured by μCT. c Relative quantification of μCT analysis. d Histomorphometric analysis of calvarial defects in mice. Arrows indicate the distance between double calcein labeling. Scale bars, 20 μm. Relative histomorphometric quantification of the mineral apposition rate (MAR) is shown (right). e Representative images of M&T staining of calvarial bone sections in mice. Scale bars, 200 μm. *New bone. f Immunohistochemistry analysis using an antibody against human vimentin and IgG control of calvarial bone sections in mice. Scale bars, 20 μm. g Immunohistochemistry analysis of USP53 (phycoerythrin [PE]; red fluorescence) and OCN (fluorescein isothiocyanate [FITC]; green fluorescence) with DAPI counterstaining of the calvarial defects in mice (left). Quantification of IHC analysis (right). Scale bars, 50 μm. Results are presented as means ± SDs. ns: not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 by one-way ANOVA. n = 5 per group.