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Adrenergic receptors mediate stress-induced elevations in extracellular Hsp72
Abstract
Heat-shock protein concentrations in the blood increase after exposure to a variety of stressors, including trauma and psychological stress. Although the physiological function of extracellular heat shock protein remains controversial, there is evidence that extracellular heat shock protein 72 (Hsp72) can facilitate immunologic responses. The signal(s) that mediate(s) the in vivo elevation of extracellular Hsp72 in the blood after stressor exposure remain(s) unknown. Here we report that Hsp72 increases in the circulation via an α 1-adrenergic receptor-mediated signaling pathway. Activation of α 1-adrenoceptors results in a rapid increase in circulating Hsp72, and blockade of α 1-adrenoceptors prevents the stress-induced rise in circulating Hsp72. Furthermore, our studies exclude a role for β-adrenoceptors, glucocorticoids, and ACTH in mediating stress-induced 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 exacerbation of inflammatory diseases during stress.
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“the release of Hsp72 (a possible DAMP) after tailshock is dependent on α-adrenergic, but not βor glucocorticoid, receptor signaling (Johnson et al, 2005;Johnson and Fleshner, 2006).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Johnson et al, 2005
In the citing paper
“For example, activation of the classical HPA and ANS stress axes can support or suppress inflammatory and adaptive immune responses in human and animal models, depending, among other factors, on whether it occurs before or after the immunological challenge (274, 371, 474).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [274]
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The Sleep-Immune Crosstalk in Health and Disease
Besedovsky, L., Lange, T., & Haack, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00010.2018 · Cited by 1,479
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Metadata
- Authors
- Johnson, J. D., Campisi, J., Sharkey, C. M., Kennedy, S. L., Nickerson, M., & Fleshner, M.
- Affiliations
- University of Colorado Boulder (US)
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2005-11
- Volume
- 99
- Issue
- 5
- Pages
- 1789-1795
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2121195298
- Cited by
- 108
- References
- 51
- Citations by year
- 2026: 4 · 2024: 3 · 2023: 3 · 2022: 2 · 2020: 5 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 6 · 2015: 6 · 2014: 5 · 2013: 6 · 2012: 12
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Health Sciences › Medicine › Physiology (medical) › Thermoregulation and physiological responses
- Keywords
- HSP72, alpha1-adrenoceptors, stress response, psychological stress, trauma (physical injury), beta-adrenergic receptors, glucocorticoids, ACTH, immunomodulation, inflammatory diseases
- MeSH terms
- Adrenalectomy, Adrenocorticotropic Hormone, Animals, Catecholamines, Electroshock, Extracellular Space, Glucocorticoids, Hypophysectomy, Immune System, Male, Rats, Inbred F344, Stress, Physiological, Tyrosine, Signal Transduction, Receptors, Adrenergic, alpha-1, HSP72 Heat-Shock Proteins, Rats
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