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16 T high static magnetic field inhibits receptor activator of nuclear factor kappa-Β ligand-induced osteoclast differentiation by regulating iron metabolism in Raw264.7 cells.
Journal of Tissue Engineering and Regenerative Medicine ( IF 3.3 ) Pub Date : 2019-11-06 , DOI: 10.1002/term.2973
Dandan Dong 1, 2 , Jiancheng Yang 1, 2, 3 , Gejing Zhang 1, 2 , Ting Huyan 1, 2 , Peng Shang 2, 4
Affiliation  

High static magnetic fields (HiSMFs) are usually defined as those SMFs with intensities ≥1 T. Although many studies have indicated that SMFs have positive effects on bone tissue, there were limited studies that investigate the effects of cells, including osteoclasts, to illustrate the effect of HiSMF on osteoclast differentiation, and whether iron involve in the altered osteoclast formation and resorption ability under HiSMF. 16 T HiSMF generated from a superconducting magnet was used. Osteoclastogenesis, bone resorption, acting ring formation, messenger ribonucleic acid expression, and protein expression were determined by tartrate-resistant acid phosphatase staining, pits formation assay, rhodamine-conjugated phalloidine staining, quantitative real-time polymerase chain reaction, and western blot, respectively. The changes induced by HiSMF in the level of iron and the concentration of mitochondrial protein, adenosine triphosphate, reactive oxygen species, malonaldehyde, and glutathione were examined by atomic absorption spectrometry and corresponding commercial kits, respectively. The results showed that HiSMF significantly inhibited osteoclastic formation and resorption ability and reduced cellular iron content during osteoclast differentiation. Mitochondrial concentration and oxidative stress levels in osteoclasts were decreased under HiSMF. Mechanistically, HiSMF markedly blocked the expression of osteoclast-associated transcription factors and osteoclast marker genes and inhibited iron absorption and iron storage-related protein expression. These findings demonstrated that the effect of HiSMF on iron metabolism of osteoclasts was involved in the inhibition of HiSMF on osteoclast differentiation.

中文翻译:

16 T高静磁场通过调节Raw264.7细胞中的铁代谢来抑制核因子kappa-Β配体诱导的破骨细胞分化的受体激活剂。

高静磁场(HiSMF)通常定义为强度≥1T的那些SMF。尽管许多研究表明SMF对骨组织有积极作用,但为研究细胞(包括破骨细胞)的作用进行的有限研究仍在进行中。抑制HiSMF对破骨细胞分化的影响,以及铁是否参与HiSMF作用下破骨细胞形成和吸收能力的改变。使用了由超导磁体产生的16 T HiSMF。分别通过抗酒石酸酸性磷酸酶染色,凹坑形成分析,若丹明缀合的鬼笔环肽染色,实时定量聚合酶链反应和蛋白质印迹法测定破骨细胞生成,骨吸收,作用环形成,信使核糖核酸表达和蛋白质表达。 。分别通过原子吸收光谱法和相应的市售试剂盒检测了HiSMF诱导的铁含量和线粒体蛋白,三磷酸腺苷,活性氧,丙二醛和谷胱甘肽浓度的变化。结果表明,HiSMF显着抑制破骨细胞分化过程中的破骨细胞形成和吸收能力,并降低细胞铁含量。在HiSMF下,破骨细胞的线粒体浓度和氧化应激水平降低。从机制上讲,HiSMF显着阻断破骨细胞相关转录因子和破骨细胞标记基因的表达,并抑制铁吸收和铁存储相关蛋白的表达。
更新日期:2019-11-06
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