ArticleDiagnostic pathology2016
Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury.
Article in Diagnostic pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 15 citations in OpenAlex.
- Aryl hydrocarbon receptor regulates programmed cell death in diseases: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- The aryl hydrocarbon receptor is expressed in non-sensory cells in the cochlea and regulates hair cell survival.Frontiers in molecular neuroscience · 2026Article
- The Aryl Hydrocarbon Receptor in Neurotoxicity: An Intermediator Between Dioxins and Neurons in the Brain.Toxics · 2025Review
- Pathways to the Brain: Impact of Fine Particulate Matter Components on the Central Nervous System.Antioxidants (Basel, Switzerland) · 2025Review
- 3,3'-Diindolylmethane improves pathology and neurological outcome following traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Melatonin Ameliorate neuroinflammation in activated microglia through the Aryl hydrocarbon-Nrf2 axis.International journal of biological sciences · 2025Article
- A Review of the Evidence for Tryptophan and the Kynurenine Pathway as a Regulator of Stem Cell Niches in Health and Disease.International journal of tryptophan research : IJTR · 2024Review
- [Effects of enhancing the expression of aryl hydrocarbon receptor in post-traumatic mice macrophages on the inflammatory cytokine level and bactericidal ability].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Thrombin-Induced Microglia Activation Modulated through Aryl Hydrocarbon Receptors.International journal of molecular sciences · 2023Article
- Modulation of Aryl Hydrocarbon Receptor Expression Alleviated Neuropathic Pain in a Chronic Constriction Nerve Injury Animal Model.International journal of molecular sciences · 2022Article
- Inhibition of Aryl Hydrocarbon Receptor Attenuates Hyperglycemia-Induced Hematoma Expansion in an Intracerebral Hemorrhage Mouse Model.Journal of the American Heart Association · 2021Article
- The Aryl Hydrocarbon Receptor: A Mediator and Potential Therapeutic Target for Ocular and Non-Ocular Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- The aryl hydrocarbon receptor: an environmental sensor integrating immune responses in health and disease.Nature reviews. Immunology · 2019Review
- The Aryl Hydrocarbon Receptor and the Nervous System.International journal of molecular sciences · 2018Review
- Cross-talk between monocyte invasion and astrocyte proliferation regulates scarring in brain injury.EMBO reports · 2018Article
- The Protective Effect of IDO1 Inhibition in Aβ-Treated Neurons and APP/PS1 Mice.American journal of Alzheimer's disease and other dementiasArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAryl Hydrocarbon Receptor (AhR) is a ligand-activated transcription factor with multiple functions operating in a variety of organs, including the brain. Recent studies have revealed that AhR played a functional role in traumatic injuries. This paper aims to study the expression of AhR during the early phase following a traumatic brain injury (TBI) in rat brains by immunohistochemistry.
methodsWeight-drop induced TBI was performed in rats. The expression of AhR in brain of TBI rats were examined by immunohistochemistry.
resultsNeuron expression of AhR in the rat brains of experiment group had been upregulated since day 3 in lesional hemisphere compared to that of the control group and mainly located in the cytoplasm, indicating an inactivated state. Interestingly, the accumulation of AhR(+) non-neuron cells became significant as early as 18 h after injury, which had kept increasing until 24 h post injury and then decreased slowly. For AhR(+) non-neuron cells, the AhR mainly located in cell nucleus, indicating a reactive status. Furthermore, double staining showed that most AhR(+) non-neuron cells co-localized with W3/13, a marker for T lymphocytes, but not with ED-1 (for activated microglia/macrophages) or GFAP (for activated astrocytes), suggesting that most AhR(+) non-neuron cells were T lymphocytes.
conclusionThis is the first study concerning AhR expression in brains following TBI, and our data demonstrated that AhR was upregulated and activated in T lymphocytes following TBI. More research is needed to make a more conclusive conclusion.
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