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Diagn Pathol. 2016 Aug 9;11(1):72. doi: 10.1186/s13000-016-0522-2.

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

Author information

1
Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing, 400038, People's Republic of China.
2
Department of Neurology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.
3
Institute of Immunology, Third Military Medical University of PLA, 30 Gaotanyan Main Street, Chongqing, 400038, People's Republic of China. zhangzhiren@yahoo.com.

Abstract

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.

KEYWORDS:

Aryl hydrocarbon receptor; T lymphocytes; Traumatic brain injury

PMID:
27506546
PMCID:
PMC4977631
DOI:
10.1186/s13000-016-0522-2
[Indexed for MEDLINE]
Free PMC Article

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