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

被引:16
作者
Xu, Kai [1 ]
Yang, Zicheng [1 ]
Shi, Rongchen [1 ]
Luo, Chunxia [2 ]
Zhang, Zhiren [1 ]
机构
[1] Third Mil Med Univ PLA, Inst Immunol, 30 Gaotanyan Main St, Chongqing 400038, Peoples R China
[2] Third Mil Med Univ, Southwest Hosp, Dept Neurol, Chongqing 400038, Peoples R China
基金
中国国家自然科学基金;
关键词
Traumatic brain injury; T lymphocytes; Aryl hydrocarbon receptor; CENTRAL-NERVOUS-SYSTEM; T-CELLS; NUCLEAR TRANSLOCATOR; DIFFERENTIATION; APOPTOSIS; IMMUNITY; PROTEIN; STROKE; STEM;
D O I
10.1186/s13000-016-0522-2
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
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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页数:6
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