Soda Akira, Ikehara Toshitaka, Kinouchi Yohsuke, Yoshizaki Kazuo
Department of Physiology, Pathophysiological Preventive Medicine, Institute of Health Biosciences, University of Tokushima Graduate School, Tokushima, Japan.
J Med Invest. 2008 Aug;55(3-4):267-78. doi: 10.2152/jmi.55.267.
The effect of exposure to extremely low frequency-electromagnetic field (ELF-EMF: 3 mT, 60 Hz) on differentiation of mouse osteoblast-like MC3T3-E1 cells was examined together with addition of insulin-like growth factor I (IGF-I). As a marker of the differentiation, the cellular collagen content was determined by the absorbance of Sirius red-stained cells measured at the wavelength of 510-520 nm with an imaging microspectroscopy. Exposure to ELF-EMF increased significantly the collagen in the cells. Treatment with PD98059, an inhibitor of extracellular signal-regulated kinase 1/2 (ERK1/2) activation, reduced the collagen in all of the cells examined on control, IGF-I addition and ELF-EMF exposure, however, PD98059 did not prevent the increase in the collagen caused by ELF-EMF exposure, and IGF-I also increased the collagen in the presence of the inhibitor. When phosphatidylinositol 3-kinase (PI3K) pathway was inhibited by LY294002, the increase in collagen induced by ELF-EMF exposure was accelerated, however, the increase in collagen observed by IGF-I addition was suppressed. Treatment with SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), suppressed the increase in the collagen induced by ELF-EMF exposure, whereas IGF-I addition increased the collagen in the presence of the inhibitor. These results suggested that collagen synthesis stimulated by ELF-EMF exposure was carried out by the participation of p38 MAPK pathway, and that PI3K pathway may have the role to suppress the collagen synthesis induced by ELF-EMF exposure, and that the suppression of the PI3K pathway may allow the acceleration of the collagen synthesis.
研究了暴露于极低频电磁场（ELF-EMF：3 mT，60 Hz）对小鼠成骨样MC3T3-E1细胞分化的影响，并同时添加了胰岛素样生长因子I（IGF-I）。作为分化的标志物，通过成像显微光谱法在510-520 nm波长处测量天狼星红染色细胞的吸光度来测定细胞胶原蛋白含量。暴露于ELF-EMF显著增加了细胞中的胶原蛋白。用细胞外信号调节激酶1/2（ERK1/2）激活抑制剂PD98059处理，可降低对照、添加IGF-I和暴露于ELF-EMF的所有检测细胞中的胶原蛋白含量，然而，PD98059并不能阻止ELF-EMF暴露引起的胶原蛋白增加，并且IGF-I在存在抑制剂的情况下也增加了胶原蛋白含量。当磷脂酰肌醇3-激酶（PI3K）途径被LY294002抑制时，ELF-EMF暴露诱导的胶原蛋白增加加速，然而，添加IGF-I观察到的胶原蛋白增加受到抑制。用p38丝裂原活化蛋白激酶（p38 MAPK）抑制剂SB203580处理，可抑制ELF-EMF暴露诱导的胶原蛋白增加，而添加IGF-I在存在抑制剂的情况下增加了胶原蛋白含量。这些结果表明，ELF-EMF暴露刺激的胶原蛋白合成是通过p38 MAPK途径参与进行的，PI3K途径可能具有抑制ELF-EMF暴露诱导的胶原蛋白合成的作用，并且PI3K途径的抑制可能允许胶原蛋白合成加速。
