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. 2023 Oct 26;11:57. doi: 10.1038/s41413-023-00295-4

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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 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. 5 — Effects of MS2 on bone formation in wild-type and compound Pkd1/Wwtr1^Oc-cKO null mice. a Bone mineral density by DEXA scan. b Bone structure by micro-CT 3D images analysis. c Periosteal mineral apposition rate (MAR) by Calcein double labeling. d Osteoclast activities by TRAP immunostaining after MS2 (50 mg·kg⁻¹) treatment for 4 weeks compared to vehicle control. Data are mean ± S.D. from 6 tibias of wild-type control and compound Pkd1/Wwtr1^Oc-cKO null mice. *P < 0.05, **P < 0.01, ***P < 0.001 compared with wild-type control mice. P values were determined by 1-way ANOVA with Tukey’s multiple-comparisons test