Martínez María Antonia, Úbeda Alejandro, Moreno Jorge, Trillo María Ángeles
Servicio de Investigación-BEM, University Hospital Ramón y Cajal-IRYCIS, 28034 Madrid, Spain.
Departamento de Ingeniería Eléctrica, Electrónica y de Automatización y Física Aplicada, Technical School of Engineering and Industrial Design (ETSID), UPM, 28012 Madrid, Spain.
Int J Mol Sci. 2016 Apr 6;17(4):510. doi: 10.3390/ijms17040510.
The proliferative response of the neuroblastoma line NB69 to a 100 µT, 50 Hz magnetic field (MF) has been shown mediated by activation of the MAPK-ERK1/2 pathway. This work investigates the MF effect on the cell cycle of NB69, the participation of p38 and c-Jun N-terminal (JNK) kinases in the field-induced proliferative response and the potential involvement of reactive oxygen species (ROS) in the activation of the MAPK-ERK1/2 and -p38 signaling pathways. NB69 cultures were exposed to the 100 µT MF, either intermittently for 24, 42 or 63 h, or continuously for periods of 15 to 120 min, in the presence or absence of p38 or JNK inhibitors: SB203580 and SP600125, respectively. Antioxidant N-acetylcysteine (NAC) was used as ROS scavenger. Field exposure induced transient activation of p38, JNK and ERK1/2. The MF proliferative effect, which was mediated by changes in the cell cycle, was blocked by the p38 inhibitor, but not by the JNK inhibitor. NAC blocked the field effects on cell proliferation and p38 activation, but not those on ERK1/2 activation. The MF-induced proliferative effects are exerted through sequential upregulation of MAPK-p38 and -ERK1/2 activation, and they are likely mediated by a ROS-dependent activation of p38.
神经母细胞瘤细胞系NB69对100µT、50Hz磁场（MF）的增殖反应已表明是由MAPK-ERK1/2信号通路的激活介导的。这项工作研究了MF对NB69细胞周期的影响、p38和c-Jun N末端（JNK）激酶在磁场诱导的增殖反应中的参与情况以及活性氧（ROS）在MAPK-ERK1/2和-p38信号通路激活中的潜在作用。在存在或不存在p38或JNK抑制剂（分别为SB203580和SP600125）的情况下，将NB69培养物间歇性暴露于100µT MF 24、42或63小时，或连续暴露15至120分钟。抗氧化剂N-乙酰半胱氨酸（NAC）用作ROS清除剂。磁场暴露诱导了p38、JNK和ERK1/2的瞬时激活。由细胞周期变化介导的MF增殖效应被p38抑制剂阻断，但未被JNK抑制剂阻断。NAC阻断了磁场对细胞增殖和p38激活的影响，但未阻断对ERK1/2激活的影响。MF诱导的增殖效应是通过依次上调MAPK-p38和-ERK1/2的激活来发挥作用的，并且它们可能是由ROS依赖性的p38激活介导的。
