Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Xi'an, China.
School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Medical College of Soochow University, Suzhou, China.
Biol Trace Elem Res. 2018 Jul;184(1):214-225. doi: 10.1007/s12011-017-1161-5. Epub 2017 Oct 19.
Many studies have indicated that static magnetic fields (SMFs) have positive effects on bone tissue, including bone formation and bone healing process. Evaluating the effects of SMFs on bone cell (especially osteoblast) function and exploring the mechanism, which is critical for understanding the possible risks or benefits from SMFs to the balance of bone remodeling. Iron and magnetic fields have the natural relationship, and iron is an essential element for normal bone metabolism. Iron overload or deficiency can cause severe bone disorders including osteoporosis. However, there are few reports regarding the role of iron in the regulation of bone formation under SMFs. In this study, hypomagnetic field (HyMF) of 500 nT, moderate SMF (MMF) of 0.2 T, and high SMF (HiMF) of 16 T were used to investigate how osteoblast (MC3T3-E1) responses to SMFs and iron metabolism of osteoblast under SMFs. The results showed that SMFs did not pose severe toxic effects on osteoblast growth. During cell proliferation, iron content of osteoblast MC3T3-E1 cells was decreased in HyMF, but was increased in MMF and HiMF after exposure for 48 h. Compared to untreated control (i.e., geomagnetic field, GMF), HyMF and MMF exerted deleterious effects on osteoblast differentiation by simultaneously retarding alkaline phosphatase (ALP) activity, mineralization and calcium deposition. However, when exposed to HiMF of 16 T, the differentiation potential showed the opposite tendency with enhanced mineralization. Iron level was increased in HyMF, constant in MMF and decreased in HiMF during cell differentiation. In addition, the mRNA expression of transferrin receptor 1 (TFR1) was promoted by HyMF but was inhibited by HiMF. At the same time, HiMF of 16 T and MMF of 0.2 T increased the expression of ferroportin 1 (FPN1). In conclusion, these results indicated that osteoblast differentiation can be regulated by altering the strength of the SMF, and iron is possibly involved in this process.
许多研究表明,静磁场(SMFs)对骨组织具有积极影响,包括骨形成和骨愈合过程。评估 SMFs 对骨细胞(尤其是成骨细胞)功能的影响,并探索其机制,对于理解 SMFs 对骨重建平衡可能带来的风险或益处至关重要。铁和磁场具有天然的关系,铁是正常骨代谢所必需的元素。铁过载或缺乏会导致严重的骨骼疾病,包括骨质疏松症。然而,关于 SMFs 下铁在骨形成调节中的作用的报道很少。在这项研究中,使用了 500nT 的低磁(HyMF)、0.2T 的中磁(MMF)和 16T 的高磁(HiMF)来研究成骨细胞(MC3T3-E1)对 SMFs 的反应以及 SMFs 下成骨细胞的铁代谢。结果表明,SMFs 对成骨细胞生长没有严重的毒性作用。在细胞增殖过程中,HyMF 中成骨细胞 MC3T3-E1 细胞的铁含量降低,但暴露 48 小时后,MMF 和 HiMF 中的铁含量增加。与未经处理的对照(即地磁场,GMF)相比,HyMF 和 MMF 通过同时抑制碱性磷酸酶(ALP)活性、矿化和钙沉积,对成骨细胞分化产生有害影响。然而,当暴露于 16T 的 HiMF 时,矿化潜力显示出相反的趋势,增强了矿化。在细胞分化过程中,HyMF 中铁水平升高,MMF 中铁水平不变,HiMF 中铁水平降低。此外,HyMF 促进转铁蛋白受体 1(TFR1)的 mRNA 表达,而 HiMF 则抑制其表达。同时,16T 的 HiMF 和 0.2T 的 MMF 增加了铁蛋白 1(FPN1)的表达。总之,这些结果表明,通过改变 SMF 的强度可以调节成骨细胞分化,而铁可能参与了这一过程。