4.3 Article

Expression of aryl hydrocarbon receptor in rat brain lesions following traumatic brain injury

Journal

DIAGNOSTIC PATHOLOGY
Volume 11, Issue -, Pages -

Publisher

BIOMED CENTRAL LTD
DOI: 10.1186/s13000-016-0522-2

Keywords

Traumatic brain injury; T lymphocytes; Aryl hydrocarbon receptor

Categories

Funding

  1. National Science and Technology Major Projects of New Drugs [2012ZX09103301035]
  2. National Natural Science Foundation of China [81471190]

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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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