Induction of metallothionein by stress and its molecular mechanisms.
Induction of metallothionein by stress and its molecular mechanisms.
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发表时间：
1999
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影响因子：
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通讯作者：
S. Jacob;K. Ghoshal;J. Sheridan
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文献类型：
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作者：
S. Jacob;K. Ghoshal;J. Sheridan
本文描述了束缚应激或社会重组应激对肝脏、心脏、肺和脾中金属硫蛋白 (MT) 诱导的影响。仅 12 小时（一个周期）的束缚应力后，MT-I 和 MT-II mRNA 均升高了 30 倍。应激后 MT 蛋白的含量也会增加。 MT诱导在肝脏中最高，其次是肺、心脏和脾。在大脑的前、中和后区域也观察到 MT-I 诱导，而大脑特异性 MT-III 基因并未被压力激活。 MT mRNA 的增加与应激诱导的血清皮质酮的增加密切相关。诱导发生在转录水平并且主要由糖皮质激素受体的激活介导。九个周期的应激后，MT mRNA 恢复到对照水平。将这些已习惯的小鼠暴露于不同类型的应激（用硫酸镉或硫酸锌等重金属处理）会导致进一步的 MT 诱导。由于重金属通过激活因子 MTF-1 诱导 MT，因此不同的诱导剂激活 MT 启动子的分子机制应该不同。
This article describes the effect of restraint stress or social reorganization stress on the induction of metallothionein (MT) in the liver, heart, lung, and spleen. Both MT-I and MT-II mRNA were elevated as much as 30-fold following just 12 h (one cycle) of restraint stress. The amount of MT protein also increased following stress. The MT induction was the highest in the liver, followed by the lung, heart, and spleen. MT-I induction was also observed in the fore, mid, and hind regions of the brain whereas the brain-specific MT-III gene was not activated by stress. The increase in MT mRNA correlated well with the rise in stress-induced serum corticosterone. The induction occurred at the transcriptional level and was mediated essentially by the activation of glucocorticoid receptor. The MT mRNA returned to the control level after nine cycles of stress. Exposure of these habituated mice to a different type of stress (treatment with heavy metals such as cadmium or zinc sulfate) led to further MT induction. Because heavy metals induced MT via activation of the factor MTF-1, distinct molecular mechanisms should be responsible for the activation of MT promoter by different inducers.