ArticleJournal of neuroinflammation2021
Neuroinflammatory processes are augmented in mice overexpressing human heat-shock protein B1 following ethanol-induced brain injury.
Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 29 citations in OpenAlex.
- APOE4 drives maladaptive heterogeneity and immunometabolic responses of astrocytes.Journal of neuroinflammation · 2026Article
- Integrative analysis of single-cell and bulk transcriptome data reveals age-related immune cell alterations in primary glioblastoma associated with prognosis.Cancer immunology, immunotherapy : CII · 2025Article
- Overexpression of the human heat shock protein B1 alters obesity-related metabolic changes in a sex-dependent manner in a mouse model of metabolic syndrome.Biology of sex differences · 2025Article
- Article
- Decoding the role of large heat shock proteins in the progression of neuroinflammation-mediated neurodegenerative disorders.Neuroprotection (Chichester, England) · 2025Review
- Role of damage-associated molecular patterns in the pathogenesis and therapeutics of traumatic brain injury.Burns & trauma · 2025Review
- Characterization of obesity-related diseases and inflammation using single cell immunophenotyping in two different diet-induced obesity models.International journal of obesity (2005) · 2024Article
- Spatial transcriptomics at the brain-electrode interface in rat motor cortex and the relationship to recording quality.Journal of neural engineering · 2024Article
- Longitudinal Neuropathological Consequences of Extracranial Radiation Therapy in Mice.International journal of molecular sciences · 2024Article
- Polystyrene Nano- and Microplastic Particles Induce an Inflammatory Gene Expression Profile in Rat Neural Stem Cell-Derived Astrocytes In Vitro.Nanomaterials (Basel, Switzerland) · 2024Article
- Perspective from single-cell sequencing: Is inflammation in acute ischemic stroke beneficial or detrimental?CNS neuroscience & therapeutics · 2024Review
- Moderate ethanol exposure reduces astrocyte-induced neuroinflammatorysignaling and cognitive decline in presymptomatic APP/PS1 mice.Research square · 2023Article
- The beauty and complexity of the small heat shock proteins: a report on the proceedings of the fourth workshop on small heat shock proteins.Cell stress & chaperones · 2023Review
- Single nucleus transcriptomics of ventral midbrain identifies glial activation associated with chronic opioid use disorder.Nature communications · 2023Article
- The Small Heat Shock Protein, HSPB1, Interacts with and Modulates the Physical Structure of Membranes.International journal of molecular sciences · 2022Article
- Small Heat Shock Proteins in Retinal Diseases.Frontiers in molecular biosciences · 2022Review
- Distinct brain regional proteome changes in the rTg-DI rat model of cerebral amyloid angiopathy.Journal of neurochemistry · 2021Article
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19 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundHeat-shock protein B1 (HSPB1) is among the most well-known and versatile member of the evolutionarily conserved family of small heat-shock proteins. It has been implicated to serve a neuroprotective role against various neurological disorders via its modulatory activity on inflammation, yet its exact role in neuroinflammation is poorly understood. In order to shed light on the exact mechanism of inflammation modulation by HSPB1, we investigated the effect of HSPB1 on neuroinflammatory processes in an in vivo and in vitro model of acute brain injury.
methodsIn this study, we used a transgenic mouse strain overexpressing the human HSPB1 protein. In the in vivo experiments, 7-day-old transgenic and wild-type mice were treated with ethanol. Apoptotic cells were detected using TUNEL assay. The mRNA and protein levels of cytokines and glial cell markers were examined using RT-PCR and immunohistochemistry in the brain. We also established primary neuronal, astrocyte, and microglial cultures which were subjected to cytokine and ethanol treatments. TNFα and hHSPB1 levels were measured from the supernates by ELISA, and intracellular hHSPB1 expression was analyzed using fluorescent immunohistochemistry.
resultsFollowing ethanol treatment, the brains of hHSPB1-overexpressing mice showed a significantly higher mRNA level of pro-inflammatory cytokines (Tnf, Il1b), microglia (Cd68, Arg1), and astrocyte (Gfap) markers compared to wild-type brains. Microglial activation, and 1 week later, reactive astrogliosis was higher in certain brain areas of ethanol-treated transgenic mice compared to those of wild-types. Despite the remarkably high expression of pro-apoptotic Tnf, hHSPB1-overexpressing mice did not exhibit higher level of apoptosis. Our data suggest that intracellular hHSPB1, showing the highest level in primary astrocytes, was responsible for the inflammation-regulating effects. Microglia cells were the main source of TNFα in our model. Microglia isolated from hHSPB1-overexpressing mice showed a significantly higher release of TNFα compared to wild-type cells under inflammatory conditions.
conclusionsOur work provides novel in vivo evidence that hHSPB1 overexpression has a regulating effect on acute neuroinflammation by intensifying the expression of pro-inflammatory cytokines and enhancing glial cell activation, but not increasing neuronal apoptosis. These results suggest that hHSPB1 may play a complex role in the modulation of the ethanol-induced neuroinflammatory response.
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