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Cited by 108Heat shock proteins researchStress Responses and CortisolThermoregulation and physiological responses

Adrenergic receptors mediate stress-induced elevations in extracellular Hsp72

Johnson, John D., Campisi, Jay, Sharkey, Craig M., Kennedy, Sarah L., Nickerson, Molly, Fleshner, Monika·2005·Journal of Applied Physiology
DOI 10.1152/japplphysiol.00390.2005
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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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Crossref · 10.1152/japplphysiol.00390.2005

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49 of 49 references verified0 citation errors · 0 not checkable

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  • The release of Hsp72 after tailshock is dependent on α-adrenergic, but not β- or glucocorticoid, receptor signaling.

    “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

  • Activation of the classical HPA and ANS stress axes can support or suppress inflammatory and adaptive immune responses in human and animal models, depending on whether it occurs before or after the immunological challenge.

    “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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Authors
Johnson, J. D., Campisi, J., Sharkey, C. M., Kennedy, S. L., Nickerson, M., & Fleshner, M.
Affiliations
University of Colorado Boulder (US)
ORCID
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
DOI
10.1152/japplphysiol.00390.2005
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 › 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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