Journal of Applied Physiology AJP: Endocrinology and Metabolism
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J Appl Physiol (March 15, 2002). doi:10.1152/japplphysiol.01122.2001
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Articles in PresS, published online ahead of print March 15, 2002
J Appl Physiol, 10.1152/jap.01122.2001
Submitted on November 8, 2001
Accepted on March 8, 2002

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

Maloyan Alina1 and Michal Horowitz1*

1 Division of Physiology, The Hebrew University, Jerusalem, Israel

* To whom correspondence should be addressed. E-mail: horowitz{at}cc.huji.ac.il.

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 ß-adrenergic signaling and/or plasma thyroxin level in eliciting these features, using rats undergoing: 1. heat acclimation (AC, 34°C, 2 and 30 days); 2. AC with ß-adrenergic blockade (APROP); 3. AC maintained euthyroid (ATHY); 4. hypothyroid (CPTU); 5. hyperthyroid (CTHY); and 6. controls (C). hsp72 mRNA (RT-PCR) and HSP72 level (Western blot) were measured before and after heat stress (2 hr 41°C, rectal temperature monitored). ß-Adrenergic blockade during AC abolished HSP72 accumulation, without disrupting HSR. Low thyroxin blunted the HSR at post-transcriptional level, while thyroxin administration in CTHY and ATHY rats arrested heat stress-evoked hsp72 transcription. We conclude that ß-adrenergic signaling contributes to the high HSP72 level characterizing the AC state. Thyroxin has two opposing effects: 1.direct-repressive, on rapid hsp72 transcription following heat stress, 2.indirect-stimulatory, via ß-adrenergic signaling. Low thyroxin could account for diminished HSP72 synthesis via lower heat production and thermoregulatory set-point.




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