Journal of Applied Physiology
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J Appl Physiol (May 11, 2006). doi:10.1152/japplphysiol.00259.2006
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Submitted on February 28, 2006
Accepted on May 4, 2006

Sexual dimorphism of the intracellular Heat Shock Protein 72 response

Molly Nickerson1, Sarah L Kennedy1, John D Johnson1, and Monika Fleshner1*

1 Integrative Physiology, University of Colorado, Boulder, Colorado, United States

* To whom correspondence should be addressed. E-mail: monika.fleshner{at}colorado.edu.

ABSTRACT The majority of previous work examining stress responses has been done in males. Recently, it has become clear that the impact of stressor exposure is modulated by sex. One stress response that may be affected by sex is the induction of intracellular Hsp72, which is a stress-responsive molecular chaperone that refolds denatured proteins and promotes cellular survival. The following study compared Hsp72 in males and females and also examined if the estrous cycle altered Hsp72 induction in females. We hypothesized that females compared to males would have a constrained Hsp72 response after an acute stressor and that stress-induced Hsp72 response in females would fluctuate with the estrous cycle. Male and female F344 rats were either left in their home cage or exposed to acute tailshock stress (8-10/group). Immediately following stressor, trunk blood was collected and tissues were flash frozen. Vaginal smear and estrogen EIA were used to categorize the phase of estrous. Results show that female rats had a greater corticosterone response than males, that both males and females exhibit a stress-induced release of progesterone, and that males and females had equal levels of stress-induced circulating norepinephrine. Sexual dimorphism of the Hsp72 (ELISA) response existed in pituitary gland, mesenteric lymph nodes, and liver such that female rats had an attenuated Hsp72 response compared to males after stress. The adrenal glands, spleen, and heart did not exhibit sexual dimorphism of the Hsp72 response. The estrous cycle did not have a significant effect on basal or stress-induced Hsp72 in females.




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