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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...

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Autores principales: Xu, Kai, Yang, Zicheng, Shi, Rongchen, Luo, Chunxia, Zhang, Zhiren
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
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.
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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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