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. 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. 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. Taken together, our results suggested that SMF-based magnetotherapy might serve as an adjunctive therapeutic option for patients with osteoporosis.

中文翻译：

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适度的SMF通过促进BMSC的定向成骨分化来减轻小鼠的骨丢失

骨质疏松症是一种未经有效治疗的常见代谢性骨病。骨髓间充质干细胞（BMSC）具有分化为多种细胞类型的潜力。BMSCs的成脂分化增加或成骨分化降低可能导致骨质疏松。静磁场（SMF）是否会影响BMSC的脂肪成骨分化平衡尚不清楚。通过各种生化（RT-PCR和Western印迹），形态学（染色和光学显微镜）和micro-CT分析确定了SMF对BMSC系分化和骨质疏松发展的影响。生物信息学分析还用于探索信号传导途径。在这项研究中，我们发现SMF（0.2-0。6 T）抑制BMSCs的成脂分化，但以强度依赖的方式促进其成骨细胞分化。整个基因组RNA-seq和生物信息学分析表明，SMF（0.6 T）降低了BMSCs中PPARγ介导的基因表达，但增加了RUNX2介导的基因转录。此外，SMF显着减轻了地塞米松或全反式维甲酸在小鼠中引起的骨量损失。综上所述，我们的结果表明，基于SMF的磁疗可以作为骨质疏松患者的辅助治疗选择。SMF明显减轻了地塞米松或全反式维甲酸在小鼠中引起的骨量损失。综上所述，我们的结果表明，基于SMF的磁疗可以作为骨质疏松患者的辅助治疗选择。SMF明显减轻了地塞米松或全反式维甲酸在小鼠中引起的骨量损失。综上所述，我们的结果表明，基于SMF的磁疗可以作为骨质疏松患者的辅助治疗选择。