Abstract
The aim of the present study was to examine intracellular redistribution of the glucocorticoid receptor (GR) in rat liver cells during a 24-h time period after exposure of the animals to 41?C whole body hyperthermic stress. The level of the receptor protein in the cytoplasmic and nuclear compartments was measured by immunoblotting procedures applied to both crude cytosol and immunopurified GR, as well as by immunocytochemical analyses applied to both paraffin-embedded liver sections and unfixed nuclear smears. All the experimental approaches employed in the study provided similar results, demonstrating that the transient stress-related decline of the cytoplasmic GR observed during the first five hours after exposure of the animals to whole-body hyperthermic stress is accompanied by enhanced nuclear accumulation of the receptor. The study can contribute to a better understanding of the influence of stress on the glucocorticoid signal transduction pathway. .
Highlights
The glucocorticoid receptor (GR) is a member of the nuclear receptor superfamily and functions as an inducible transcription factor activated by hormone binding
The results demonstrate that the stress-related decline of the cytoplasmic GR observed during the first five hours after exposure of the animals to whole-body hyperthermic stress is accompanied by enhanced accumulation of the receptor in the nuclei
The level and intracellular redistribution of GR in the liver of rats exposed to 41°C whole body hyperthermic stress were determined by both immunoblotting and immunocytochemical procedures
Summary
The glucocorticoid receptor (GR) is a member of the nuclear receptor superfamily and functions as an inducible transcription factor activated by hormone binding. Glucocorticoid hormones play an indispensable role in the organismal response to stress This fact, together with evidence indicating that hormone-free GR exists in target cells in the form of multiprotein complexes with heat shock proteins (Pratt and T o f t, 1997), led researchers to explore possible connection between glucocorticoid hormone action and heat shock response. Studies along these lines were performed predominantly on cells grown in culture and have revealed that heat stress produces serious disturbances at the most important steps controlling the receptor’s function. Molecular mechanisms underlying the heat shock potentiation effect remain to be elucidated, this phenomenon is usually linked with stress-induced increase in nuclear accumulation of the receptors
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