Molecular mechanisms of glucocorticoid resistance in splenocytes of socially stressed male mice
Abstract
Splenocytes from socially stressed male mice display functional glucocorticoid (GC) resistance, viz., the antiproliferative effects of GC on lipopolysaccharide (LPS)-stimulated splenocytes is absent. In this study, we investigated changes in the structure and function of the glucocorticoid receptor (GR) in socially stressed animals. Changes of GR at both DNA and RNA levels were excluded. Reduced GR function was restricted to macrophages (CD11b(+)) in association with impaired nuclear translocation of GR after GC stimulation. Consequently, GC failed to block the activation of NF-kappa B in these cells. Thus, impaired nuclear translocation of GR and the lack of transcriptional suppression of NF-kappa B by GC were identified as the molecular mechanisms responsible for the observed GC resistance in spleens of socially stressed mice.
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The mechanism of glucocorticoid resistance in socially disrupted mice involves decreased GR translocation from cytoplasm to nucleus.
“the mechanism of glucocorticoid resistance in socially disrupted mice involves decreased GR translocation from cytoplasm to nucleus,60”
From Cytokines and Glucocorticoid Receptor Signaling (2009) · cites this paper as [60]
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- Authors
- Quan, N.
- Affiliations
- Institute for Behavioral Medicine (US)
- Corresponding author
- Quan, N
- ORCID
- Quan, N
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2003-04
- Volume
- 137
- Issue
- 1-2
- Pages
- 51-58
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W1989896761
- Cited by
- 113
- References
- 1
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 5 · 2020: 5 · 2019: 2 · 2018: 10 · 2017: 9 · 2016: 6 · 2015: 6 · 2014: 8 · 2013: 3 · 2012: 7
- FWCI
- 1.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ohio State University
- National Institutes of Health
- National Institute of Mental Health (R01MH046801, R01-MH46801)
- National Institute of Dental and Craniofacial Research (P50 DE-13749, P50DE013749)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- glucocorticoid resistance, glucocorticoid receptor, social stress, splenocytes, macrophages, CD11b, nuclear translocation, NF-κB, lipopolysaccharide, transcriptional repression, stress immunology
- MeSH terms
- Animals, B-Lymphocytes, Corticosterone, Drug Resistance, Lipopolysaccharides, Lymphocyte Activation, Macrophages, Male, Mice, Inbred C57BL, Spleen, Stress, Psychological, Mice
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