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Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury
BACKGROUND: Aryl 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 d...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4977631/ https://www.ncbi.nlm.nih.gov/pubmed/27506546 http://dx.doi.org/10.1186/s13000-016-0522-2 |
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author | Xu, Kai Yang, Zicheng Shi, Rongchen Luo, Chunxia Zhang, Zhiren |
author_facet | Xu, Kai Yang, Zicheng Shi, Rongchen Luo, Chunxia Zhang, Zhiren |
author_sort | Xu, Kai |
collection | PubMed |
description | BACKGROUND: Aryl 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. METHODS: Weight-drop induced TBI was performed in rats. The expression of AhR in brain of TBI rats were examined by immunohistochemistry. RESULTS: Neuron 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. CONCLUSION: This 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. |
format | Online Article Text |
id | pubmed-4977631 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-49776312016-08-10 Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury Xu, Kai Yang, Zicheng Shi, Rongchen Luo, Chunxia Zhang, Zhiren Diagn Pathol Research BACKGROUND: Aryl 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. METHODS: Weight-drop induced TBI was performed in rats. The expression of AhR in brain of TBI rats were examined by immunohistochemistry. RESULTS: Neuron 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. CONCLUSION: This 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. BioMed Central 2016-08-09 /pmc/articles/PMC4977631/ /pubmed/27506546 http://dx.doi.org/10.1186/s13000-016-0522-2 Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Xu, Kai Yang, Zicheng Shi, Rongchen Luo, Chunxia Zhang, Zhiren Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title | Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title_full | Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title_fullStr | Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title_full_unstemmed | Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title_short | Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
title_sort | expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4977631/ https://www.ncbi.nlm.nih.gov/pubmed/27506546 http://dx.doi.org/10.1186/s13000-016-0522-2 |
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