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J Appl Physiol 93: 107-115, 2002. First published March 15, 2002; doi:10.1152/japplphysiol.01122.2001
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Vol. 93, Issue 1, 107-115, July 2002

beta -Adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation

Alina Maloyan and Michal Horowitz

Division of Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem 91120, Israel

Heat acclimation upregulates 72-kDa heat shock protein (HSP72) and predisposes to faster activation of the heat shock response (HSR). This study investigates the role played by beta -adrenergic signaling and/or plasma thyroxine level in eliciting these features by using rats undergoing 1) heat acclimation (AC; 34°C, 2 and 30 days); 2) AC with beta -adrenergic blockade; 3) AC-maintained euthyroid; 4) hypothyroid; 5) hyperthyroid; and 6) controls. The hsp72 mRNA (RT-PCR) and HSP72 levels (Western blot) were measured before and after heat stress (2 h, 41°C, rectal temperature monitored). beta -Adrenergic blockade during AC abolished HSP72 accumulation, without disrupting HSR. Low thyroxine blunted the HSR at posttranscriptional level, whereas thyroxine administration in hyperthyroid and AC-maintained euthyroid rats arrested heat stress-evoked hsp72 transcription. We conclude that beta -adrenergic signaling contributes to the high HSP72 level characterizing the AC state. Thyroxine has two opposing effects: 1) direct repressive on rapid hsp72 transcription after heat stress; and 2) indirect stimulatory via beta -adrenergic signaling. Low thyroxine could account for diminished HSP72 synthesis via lower heat production and thermoregulatory set point.

heat shock protein; heat shock response; heat stress; hypothyroid; hyperthyroid; propranolol; beta -adrenergic receptors; heat-acclimatory homeostasis


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