ArticleBiomolecules2019
Microglia Activated by Excess Cortisol Induce HMGB1 Acetylation and Neuroinflammation in the Hippocampal DG Region of Mice Following Cold Exposure.
Article in Biomolecules, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 23 citations in OpenAlex.
- The mechanisms by which hypothalamic neuroinflammation induced by neonatal cerebral ischemia-hypoxia leads to decreased thymic function via the HPA axis.Cell & bioscience · 2026Article
- A Narrative Review on Rodent Models of Neuropsychopathology Associated with Low Temperature Exposure.Neuropsychiatric disease and treatment · 2026Review
- Neuroinflammatory Loop in Schizophrenia, Is There a Relationship with Symptoms or Cognition Decline?International journal of molecular sciences · 2025Review
- Early-life obesogenic environment integrates immunometabolic and epigenetic signatures governing neuroinflammation.Brain, behavior, & immunity - health · 2024Article
- Mechanisms underlying delirium in patients with critical illness.Frontiers in aging neuroscience · 2024Review
- Melatonin modulates neuroinflammatory response and microglial activation in mice exposed to dim blue light at night.Frontiers in pharmacology · 2024Article
- Neurodevelopmental and Neuropsychiatric Disorders.Advances in neurobiology · 2024Review
- Biological Pathways Associated with Vitamins in Autism Spectrum Disorder.Neurotoxicity research · 2023Review
- Article
- Supplementary Pharmacotherapy for the Behavioral Abnormalities Caused by Stressors in Humans, Focused on Post-Traumatic Stress Disorder (PTSD).Journal of clinical medicine · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cold stress can induce neuroinflammation in the hippocampal dentate gyrus (DG), but the mechanism underlying neuronal apoptosis induced by cold stress is not well-understood. To address this issue, male and female C57BL/6 mice were exposed to a temperature of 4 °C for 3 h per day for 1 week, and glial cell activation, neuronal apoptosis, and neuroinflammation were evaluated by western blotting, immunofluorescence, terminal deoxynucleotidyl transferase 2'-deoxyuridine 5'-triphosphate (dUTP) nick end labeling, Nissl staining, and immunohistochemistry. Additionally, BV2 cells were treated with different concentrations of cortisol (CORT) for 3 h to mimic stress and molecular changes were assessed by western blotting, immunofluorescence, and co-immunoprecipitation. We found that excess CORT activated glial cells and increased neuroinflammation in the DG of mice exposed to cold temperatures, which was associated with increased acetylation and nuclear factor-κB signaling. These effects were mediated by the acetylation of lysine 9 of histone 3 and lysine 310 of p65, which resulted in increased mitogen-activated protein kinase phosphorylation, nuclear translocation of p65, microglia activation, and acetylation of high-mobility group box 1. Neuroinflammation was more severe in male compared to female mice. These findings provide new insight into the mechanisms of the cold stress response, which can inform the development of new strategies to combat the effects of hypothermia.
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Registered trials
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