Moderate SMFs attenuate bone loss in mice by promoting directional osteogenic differentiation of BMSCs
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RESEARCH
Open Access
Moderate SMFs attenuate bone loss in mice by promoting directional osteogenic differentiation of BMSCs Guilin Chen1†, Yujuan Zhuo1†, Bo Tao2†, Qian Liu1, Wenlong Shang1, Yinxiu Li1, Yuhong Wang1, Yanli Li1, Lei Zhang3, Yanwen Fang4, Xin Zhang3, Zhicai Fang4 and Ying Yu1*
Abstract Background: Osteoporosis is a common metabolic bone disease without effective treatment. Bone marrow-derived mesenchymal stem cells (BMSCs) have the potential to differentiate into multiple cell types. Increased adipogenic differentiation or reduced osteogenic differentiation of BMSCs might lead to osteoporosis. Whether static magnetic fields (SMFs) might influence the adipo-osteogenic differentiation balance of BMSCs remains unknown. Methods: The effects of SMFs on lineage differentiation of BMSCs and development of osteoporosis were determined by various biochemical (RT-PCR and Western blot), morphological (staining and optical microscopy), and micro-CT assays. Bioinformatics analysis was also used to explore the signaling pathways. Results: In this study, we found that SMFs (0.2–0.6 T) inhibited the adipogenic differentiation of BMSCs but promoted their osteoblastic differentiation in an intensity-dependent manner. Whole genomic RNA-seq and bioinformatics analysis revealed that SMF (0.6 T) decreased the PPARγ-mediated gene expression but increased the RUNX2-mediated gene transcription in BMSCs. Moreover, SMFs markedly alleviated bone mass loss induced by either dexamethasone or all-trans retinoic acid in mice. Conclusions: Taken together, our results suggested that SMF-based magnetotherapy might serve as an adjunctive therapeutic option for patients with osteoporosis. Keywords: Bone marrow-derived mesenchymal stem cell, Static magnetic field, Osteoporosis, Osteogenic differentiation, Magnetic therapy
* Correspondence: [email protected] † Guilin Chen, Yujuan Zhuo, and Bo Tao contributed equally to this work and should be regarded as joint first authors. 1 Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China Full list of author information is available at the end of the article © The Author(s). 2020 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 permissi
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