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. 2018 Jun 1;9:2143. doi: 10.1038/s41467-018-04464-6

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Tet DKO mice show BMMSC impairment. a Toluidine blue staining showed the CFU-F in control, Tet1^−/−, Prx1^creTet2^fl/fl, and Tet DKO BMMSCs. b BrdU-labeling assay showed the proliferation rate in control, Tet1^−/−, Prx1^creTet2^fl/fl, and Tet DKO BMMSCs. c, d When cultured under osteogenic inductive conditions, the capacities to form mineralized nodules of control, Tet1^−/−, Prx1^creTet2^fl/fl, and Tet DKO BMMSCs were assessed by alizarin red staining (c), and the expression of osteogenic markers Runx2, ALP and OCN, as were assessed by western blotting (d). e New bone (B) formation of control, Tet1^−/−, Prx1^creTet2^fl/fl, and Tet DKO BMMSCs when subcutaneously implanted into immunocompromised mice with hydroxyapatite tricalcium phosphate (HA/TCP; HA) as a carrier. *p < 0.05, **p < 0.01, ***p < 0.001 (mean ± SD). Scale bar, 50 μm. Results are from three independent experiments. p values were calculated using one-way ANOVA