ArticleBrain, behavior, and immunity2015
Molecular mechanisms of repeated social defeat-induced glucocorticoid resistance: Role of microRNA.
Article in Brain, behavior, and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- A Vortioxetine-Glycyrrhizic Acid Supramolecular Complex: Synthesis and Cellular Effects on Microglial and Blood Cells Under Inflammatory and Glucocorticoid Challenge.Biomedicines · 2026Article
- Epigenetic mechanisms and steroid-resistant nephrotic syndrome: The future potential for SRNS diagnosis.iScience · 2026Review
- Genetic heritage of war: exploring transgenerational inheritance of PTSD and its molecular background.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Glucocorticoid receptor dynamics and neuroinflammation in chronic restraint stress-induced mechanical allodynia in female rats.The journal of pain · 2025Article
- Convergence of endothelial dysfunction, inflammation and glucocorticoid resistance in depression-related cardiovascular diseases.BMC immunology · 2024Review
- Role of microRNAs and long non‑coding RNAs in glucocorticoid signaling (Review).International journal of molecular medicine · 2022Review
- Cause or consequence? Understanding the role of cortisol in the increased inflammation observed in depression.Current opinion in endocrine and metabolic research · 2022Article
- Review
- MicroRNAs in Basolateral Amygdala Associated with Stress and Fear Memories Regulate Rapid Eye Movement Sleep in Rats.Brain sciences · 2021Article
- HPA axis regulation and epigenetic programming of immune-related genes in chronically stressed and non-stressed mid-life women.Brain, behavior, and immunity · 2021Article
- Enduring neuroimmunological consequences of developmental experiences: From vulnerability to resilience.Molecular and cellular neurosciences · 2020Review
- A review of epigenetic contributions to post-traumatic stress disorder .Dialogues in clinical neuroscience · 2019Review
- The biological embedding of neonatal stress exposure: A conceptual model describing the mechanisms of stress-induced neurodevelopmental impairment in preterm infants.Research in nursing & health · 2019Article
- Disease- and treatment-associated acquired glucocorticoid resistance.Endocrine connections · 2018Review
- Chronic social stress induces DNA methylation changes at an evolutionary conserved intergenic region in chromosome X.Epigenetics · 2018Article
- Aggression, Social Stress, and the Immune System in Humans and Animal Models.Frontiers in behavioral neuroscience · 2018Review
- Splenic glucocorticoid resistance following psychosocial stress requires physical injury.Scientific reports · 2017Article
- Checks and balances: The glucocorticoid receptor and NFĸB in good times and bad.Frontiers in neuroendocrinology · 2017Review
- The effects of microRNAs on glucocorticoid responsiveness.Journal of cancer research and clinical oncology · 2017Review
- Repeated Social Defeat, Neuroinflammation, and Behavior: Monocytes Carry the Signal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.