Molecular mechanisms of repeated social defeat-induced glucocorticoid resistance: Role of microRNA
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Glucocorticoid (GC) resistance is a severe problem associated with various inflammatory diseases. Previous studies have shown that repeated social stress induces GC resistance in innate immune cells, but the underlying molecular mechanisms have not been fully elucidated. Therefore, the purpose of this study was to examine potential underlying molecular mechanism(s) of repeated social defeat (RSD) stress on GC resistance in splenic macrophages. It was hypothesized that mRNA expression of receptors for GC and nuclear translocating-associated regulators in splenic macrophages would be affected by RSD, and that these changes would be associated with epigenetic modification. The data showed that the mRNA expression of GC and mineralocorticoid receptors were significantly decreased in splenic macrophages by RSD. RSD also induced a significantly decreased mRNA expression in FK506-binding protein 52 (FKBP52), consequently resulting in a significantly increased ratio of FKBP51 to FKBP52. Moreover, DNA methyltransferases 3a and 3b showed a significant decrease in their mRNA expression in the RSD group as did mRNA expression of histone deacetyltransferase 2. The RSD group also showed a significantly reduced quantity of methylated DNA in splenic macrophages. Based on microRNA (miRNA) profiling data, it was determined that RSD induced significantly increased expression of 9 different miRNAs that were predicted to interact with mRNAs of the GC receptor (6 miRNAs), mineralocorticoid receptor (3 miRNAs) and FKBP52 (2 miRNAs). Spearman correlation analysis revealed significantly strong correlations between the expression of 2 miRNAs and their target mRNA expression for GC receptors. Among these miRNAs, we verified direct effects of miRNA-29b and -340 overexpression on mRNA expression of GC receptors in L929 cells. The overexpression of miRNA-29b or -340 in L929 cells significantly reduced LPS-induced overexpression of GC receptors. In conclusion, this study provides evidence that epigenetic regulation, such as DNA methylation and miRNA expression, may play a role in the RSD-induced GC resistance that we have observed in splenic macrophages.
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GC resistance is likely mediated by loss of anti-inflammatory feedback from the GC receptor, involving impaired GC receptor translocation and decreased FKBP52.
“GC resistance is likely mediated by loss of anti-inflammatory feedback from the GC receptor.”
From Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal (2017) · cites this paper as Jung et al, 2015
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Psychosocial Impact of Epigenetics in Pediatrics
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Topol, I. A., & Kamyshnyi, A. (2015) · Experimental and Clinical Physiology and Biochemistry · doi:10.25040/ecpb2015.03.007
- Authors
- Jung, S. H., Wang, Y., Kim, T., Tarr, A., Reader, B., Powell, N., & Sheridan, J. F.
- Affiliations
- The Ohio State University Wexner Medical Center (US)
- Vanderbilt University Medical Center (US)
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 44
- Pages
- 195-206
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC4275324
- OpenAlex
- W1999798541
- Cited by
- 47
- References
- 46
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 3 · 2018: 8 · 2017: 8 · 2016: 8 · 2015: 5
- FWCI
- 3.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH/NIMH (R01MH093473, R01MH097243)
- NIDCR (T32DE014320)
- 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, repeated social defeat, social stress, splenic macrophages, microRNA, DNA methylation, mineralocorticoid receptor, glucocorticoid receptor, FKBP52, FKBP51, HDAC2, DNA methyltransferases, epigenetic regulation, miR-29b, miR-340, innate immunity
- MeSH terms
- Tacrolimus Binding Protein 5, Animals, Macrophages, Male, Mice, Inbred C57BL, Receptors, Glucocorticoid, RNA, Messenger, Social Behavior, Spleen, Stress, Psychological, Receptors, Mineralocorticoid, DNA Methylation, Tacrolimus Binding Proteins, MicroRNAs, Epigenesis, Genetic
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