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. 2022 Jan 7;10:3. doi: 10.1038/s41413-021-00171-z

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© The Author(s) 2022

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. 4 — E2 increased BMP2 and HOXC6 expression in DMSCs through the recruitment of KDM6B to promoters and removal of H3K27me3 marks. Occupancy of KDM6B at the BMP2 (a) and HOXC6 (b) promoters, as determined by ChIP, upon E2 treatment. Occupancy of H3K27me3 at the BMP2 (c) and HOXC6 (d) promoters, as determined by ChIP, upon E2 treatment. Occupancy of KDM6B at the BMP2 (e) and HOXC6 (f) promoters in the control and KDM6B-depleted DMSCs, as determined by ChIP, upon E2 treatment. Occupancy of H3K27me3 at the BMP2 (g) and HOXC6 (h) promoters in the control and KDM6B-depleted DMSCs, as determined by ChIP, upon E2 treatment. Data are presented as the mean ± SEM (n = 3). All the groups were compared by two-way ANOVA with Bonferroni post hoc test. Asterisks were assigned to P values with statistical significance (*P < 0.05; **P < 0.01; ***P < 0.001)