β-adrenergic signaling and thyroid hormones affect HSP72 expression during heat acclimation

Alina Maloyan, Michal Horowitz

Research output: Contribution to journalArticle

47 Scopus citations

Abstract

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 β-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 β-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). β-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 β-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 β-adrenergic signaling. Low thyroxine could account for diminished HSP72 synthesis via lower heat production and thermoregulatory set point.

Original languageEnglish (US)
Pages (from-to)107-115
Number of pages9
JournalJournal of applied physiology
Volume93
Issue number1
DOIs
StatePublished - 2002

Keywords

  • Heat shock protein
  • Heat shock response
  • Heat stress
  • Heat-acclimatory homeostasis
  • Hyperthyroid
  • Hypothyroid
  • Propranolol
  • β-adrenergic receptors

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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