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. Author manuscript; available in PMC: 2016 Oct 6.
Published in final edited form as: Cell Metab. 2015 Sep 10;22(4):606–618. doi: 10.1016/j.cmet.2015.08.018

Figure 1. MSC transplantation (MSCT) rescued impaired BMMSC functions and osteoporotic phenotype in MRL/lpr mice via regulation of DNA methylation profile.

Figure 1

(A) Alizarin red staining showed mineralized nodule formation of BMMSCs derived from wild-type C3H/HeJ mice (C3H/HeJ), MRL/lpr mice (MRL/lpr) and MRL/lpr mice at 4 weeks post-MSCT. n = 5. Western blot showed expression of Runx2 and ALP in BMMSCs. β-Actin was used as a loading control. (B) H&E staining showed formation of new bone (B) and bone marrow (BM) around HA/TCP (HA) carrier when BMMSCs were implanted into immunocompromised mice. n = 5. (C) μCT analysis of bone mineral density (BMD) and bone volume/total volume (BV/TV) of femurs. n = 5. (D) MA plot showed global methylation patterns of gene promoters in BMMSCs, as assessed by DNA methylation microarray. (E) Alizarin red staining showed mineralized nodule formation by BMMSCs. n = 5. Western blot showed expressions of Runx2 and ALP in BMMSCs. (F) H&E staining showed formation of new bone (B) and bone marrow (BM) around HA/TCP (HA) carrier when BMMSCs were implanted into immunocompromised mice. n = 5. (G) μCT analysis of BMD and BV/TV of femurs. n = 5. All results are representative of data generated in three independent experiments except DNA methylation microarray analysis. Statistical significance was determined with one-way analysis of variance (ANOVA). **P < 0.01; *P < 0.05. Error bars: mean ± SD; 200 μm (B, F), 1 mm (C, G).