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. 2022 Apr 1;54(4):483–492. doi: 10.1038/s12276-022-00749-5

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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. 5 — a ARS results showed that the osteogenic differentiation ability of CMKLR1⁺ MSCs was stronger than that of CMKLR1⁻ MSCs. b ALP assays showed that the osteogenic differentiation ability of CMKLR1⁺ MSCs was stronger than that of CMKLR1⁻ MSCs. c ORO staining and quantitative results demonstrated that the adipogenic differentiation ability of CMKLR1⁺ MSCs was weaker than that of CMKLR1⁻ MSCs. d H&E and Masson staining showed that more new bone formation was observed in the CMKLR1⁺ MSC group than in the CMKLR1⁻ MSC group in vivo. More OCN⁺ osteoblasts were also observed in the CMKLR1⁺ MSC group than in the CMKLR1⁻ MSC group in vivo. e H&E staining and perilipin-1 staining showed that the number of adipocytes in the CMKLR1⁺ MSC group was less than that in the CMKLR1⁻ MSC group in vivo.