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J Appl Physiol (July 21, 2005). doi:10.1152/japplphysiol.00390.2005
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Submitted on April 7, 2005
Accepted on July 14, 2005

Adrenergic Receptors Mediate Stress-Induced Elevations in Extracellular Hsp72

John D Johnson1*, Jay Campisi1, Craig M Sharkey1, Sarah L Kennedy1, Molly Nickerson1, and Monika Fleshner1

1 Department of Integrative Physiology & Center for Neuroscience, University of Colorado, Boulder, CO, USA

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

Heat-shock proteins (Hsp) concentrations elevate in the blood after exposure to a variety of stressors, including trauma and psychological stress. Although the physiological function of extracellular Hsp remains controversial, there is evidence that extracellular Hsp 72 can facilitate immunological responses. What remains unknown is what signal(s) mediates the in vivo elevation of extracellular Hsp72 in the blood after stressor exposure. Here we report that Hsp72 elevates in the circulation via an {alpha}1 - adrenergic receptor mediated signaling pathway. Activation of {alpha}1 -adrenoceptors results in a rapid increase in circulating Hsp72 and blockade of {alpha}1 -adrenoceptors prevents the stress-induced rise in circulating Hsp72. Furthermore, our studies exclude a role for {beta}-adrenoceptors, glucocorticoids, and adrenocorticotropin hormone in mediating stressinduced elevations in circulating extracellular Hsp72. Understanding the signals involved in elevating extracellular Hsp72 could facilitate the use of extracellular Hsp72 to bolster immunity and perhaps prevent the exacerbation of inflammatory diseases during times of stress.




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