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

Maloyan, Alina, and Michal Horowitz. -Adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation. J Appl Physiol 93: 107–115, 2002. First published March 15, 2002; 10.1152/japplphysiol.01122. 2001.—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 -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 -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). -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 -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 -adrenergic signaling. Low thyroxine could account for diminished HSP72 synthesis via lower heat production and thermoregulatory set point.