Lin H, Han L, Blank M, Head M, Goodman R
Department of Pathology, Columbia University Health Sciences, New York, New York 10032, USA.
J Cell Biochem. 1998 Sep 1;70(3):297-303.
The mechanisms involved in sensing, signaling, and coordinating changes resulting from magnetic field-induced stress show substantial similarities to those of heat shock, e.g., magnetic field-induced heat shock 70 gene (HSP70) expression involves heat shock factor (HSF) activation and heat shock element binding. However, an additional requirement for transactivation of HSP70 expression by magnetic fields is the binding of Myc protein, indicating that additional elements and/or pathways are involved in the induction of HSP70 expression by magnetic fields. To investigate the possible participation of additional genetic elements in magnetic field-induced HSP70 expression, we examined both magnetic field exposure and heat shock on protein-DNA binding of the transcription factors HSF, AP-1, AP-2, and SP-1 in four human cell lines. The binding sites for these transcription factors are present in the HSP70 promoter. AP-1 binding activity, normally not increased by heat shock, was increased by magnetic fields; heat shock induced an increase only in HSF binding. Although intersecting and converging signaling pathways could account for the multiplicity of elements involved in magnetic field-induced HSP70 transcription, direct interaction of magnetic fields with DNA is also a possible mechanism. Because magnetic fields penetrate the cell, they could well react with conducting electrons present in the stacked bases of the DNA.
磁场诱导应激所涉及的感知、信号传导及协调变化机制,与热休克机制存在显著相似性,例如,磁场诱导的热休克70基因(HSP70)表达涉及热休克因子(HSF)激活及热休克元件结合。然而,磁场对HSP70表达进行反式激活的一个额外要求是Myc蛋白的结合,这表明磁场诱导HSP70表达还涉及其他元件和/或信号通路。为研究其他遗传元件在磁场诱导HSP70表达中可能的参与情况,我们检测了四种人类细胞系中磁场暴露及热休克对转录因子HSF、AP-1、AP-2和SP-1蛋白-DNA结合的影响。这些转录因子的结合位点存在于HSP70启动子中。通常热休克不会增加的AP-1结合活性,却因磁场而增加;热休克仅诱导HSF结合增加。尽管交叉和汇聚的信号通路可解释磁场诱导HSP70转录所涉及元件的多样性,但磁场与DNA的直接相互作用也是一种可能机制。由于磁场可穿透细胞,它们很可能与DNA堆积碱基中存在的传导电子发生反应。