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. 2023 Jul 10;14:4091. doi: 10.1038/s41467-023-39744-3

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — a Immunostaining images showed the upregulated expression of RUNX2 in the CSCM-M group after 3 and 7 days of cell culture (Scale bars: 50 µm). b Rt-qPCR analysis of upregulation of canonical osteogenic markers (Runx2, Smad1, Sp7, Colα1) in the CSCM-M group. n = 3 biologically independent samples; mean ± SEM.*P < 0.05, one-way ANOVA. c Western blot analysis revealed the upregulation of canonical osteogenic markers (BMP2, RUNX2, OPN) in the CSCM-M group. d The timeline of magnetic field loading for the in vivo experiment. Created with BioRender.com. e Micro-CT images, bone volume statistics, and H&E staining of tissue sections f of bone defect repair after 4 and 8 weeks after CSCM and CCM implantation within skull defect in rats. NB new bone. n = 3 rats for per group and per time point; mean ± SEM. *P < 0.05, one-way ANOVA. Source data are provided as a Source Data file. At least three times of experiments were repeated independently.