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J Biol Chem, Vol. 273, Issue 43, 27904-27910, October 23, 1998
From the Departments of Metallothioneins (MT) have been implicated in the
protection of cells from oxidative stress. We studied the molecular
mechanism of induction of MT-I and MT-II in response to restraint
stress using a mouse model system in which the animals were restrained in well ventilated polypropylene tubes for 12 h each day (one cycle). Here, we show that MT-I and MT-II mRNA levels were elevated as much as 10-20-fold after just one cycle of this simple stress. Stress-mediated MT induction occurred at the transcriptional level. The
level of MT mRNA correlated with the stress-induced increase, and
not with the diurnal variation, in the level of serum glucocorticoid. Treatment of the mice with RU 486, a glucocorticoid receptor
antagonist, prior to restraint stress inhibited MT induction by at
least 50%. Furthermore, the glucocorticoid responsive element-binding
activity in the liver nuclear extracts from the stressed mice was
significantly higher than that in the control mice. The complex
formations between the transcription factor Sp1, MTF1, or MLTF/ARE and
the respective specific oligonucleotides were not altered in the liver
from the stressed mouse. The MT mRNA levels returned to the basal
level at the end of nine cycles of stress, indicating habituation of the animals to restraint stress. At this stage, exposure of the animals
to another type of stress, treatment with heavy metals, resulted in
further induction of MT. These data indicate that glucocorticoid is the
primary physiological factor responsible for MT induction following
restraint stress, and the glucocorticoid receptor is the major
transcription factor involved in this process.
Metallothionein Induction in Response to Restraint Stress
TRANSCRIPTIONAL CONTROL, ADAPTATION TO STRESS, AND ROLE OF
GLUCOCORTICOID
,,
, and§
Medical Biochemistry and
Medical Microbiology and Immunology and the
§ Comprehensive Cancer Center,
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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