Key Laboratory for Space Biosciences and Biotechnology, Institute of Special Environment Biophysics, School of Life Sciences, Northwestern Polytechnical University, Xi'an, China.
Institute of Flexible Electronics (IFE), Northwestern Polytechnical University, 127 Youyi Xilu, Xi'an, 710072 Shaanxi, China.
Biomed Res Int. 2020 Mar 26;2020:5762932. doi: 10.1155/2020/5762932. eCollection 2020.
The magnetic field is the most common element in the universe, and high static magnetic field (HiSMF) has been reported to act as an inhibited factor for osteoclasts differentiation. Although many studies have indicated the negative role of HiSMF on osteoclastogenesis of RANKL-induced RAW264.7 cells, the molecular mechanism is still elusive. In this study, the HiSMF-retarded cycle and weakened differentiation of RAW264.7 cells was identified. Through RNA-seq analysis, RANKL-induced RAW264.7 cells under HiSMF were analysed, and a total number of 197 differentially expressed genes (DEGs) were discovered. Gene ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that regulators of cell cycle and cell division such as Bub1b, Rbl1, Ube2c, Kif11, and Nusap1 were highly expressed, and CtsK, the marker gene of osteoclastogenesis was downregulated in HiSMF group. In addition, pathways related to DNA replication, cell cycle, and metabolic pathways were significantly inhibited in the HiSMF group compared to the Control group. Collectively, this study describes the negative changes occurring throughout osteoclastogenesis under 16 T HiSMF treatment from the morphological and molecular perspectives. Our study provides information that may be utilized in improving magnetotherapy on bone disease.
磁场是宇宙中最常见的元素，已有研究报道，高静磁场（HiSMF）可作为破骨细胞分化的抑制因子。虽然许多研究表明 HiSMF 对 RANKL 诱导的 RAW264.7 细胞破骨细胞生成具有负向作用，但其中的分子机制仍不清楚。在本研究中，我们发现 HiSMF 会延缓 RAW264.7 细胞的周期并减弱其分化。通过 RNA-seq 分析，我们对 HiSMF 下 RANKL 诱导的 RAW264.7 细胞进行了分析，共发现 197 个差异表达基因（DEGs）。基因本体（GO）富集分析和京都基因与基因组百科全书（KEGG）通路分析表明，细胞周期和细胞分裂的调节因子如 Bub1b、Rbl1、Ube2c、Kif11 和 Nusap1 表达上调，而破骨细胞生成的标记基因 CtsK 在 HiSMF 组中表达下调。此外，与 DNA 复制、细胞周期和代谢途径相关的通路在 HiSMF 组中与对照组相比明显受到抑制。综上所述，本研究从形态学和分子水平描述了 16T HiSMF 处理下破骨细胞生成过程中发生的负向变化。我们的研究为利用磁疗改善骨骼疾病提供了信息。
