Upregulation of Interferon Regulatory Factor 6 Promotes Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats

被引:0
作者
Yuchang Lin
Dezhi Xu
Xiaohong Li
Chun Liu
Xia Liu
Shen Huang
Yuwei Huang
Xiaojuan Liu
机构
[1] Wuxi Second Hospital Affiliated to Nanjing Medical University,Department of Neurosurgery
[2] Affiliated Hospital of Nantong University,Surgical Comprehensive Laboratory
[3] Nantong University,Laboratory Animal Center
[4] Nantong University,Department of Pathophysiology, Medical College
[5] Nantong University,Department of Osteology, Second Affiliated Hospital
[6] Nantong University,Institute of Navigation Medicine
[7] Nantong University,Department of Pathogen Biology, Medical College
[8] Nantong University,Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Medical College
来源
Cellular and Molecular Neurobiology | 2016年 / 36卷
关键词
IRF6; Traumatic brain injury; Neuronal apoptosis; Rat;
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学科分类号
摘要
The interferon regulatory factor (IRF) family was first discovered as a set of transcriptional regulators of the type I interferon system in 1988. In mammals, the IRF family includes nine members that play important roles in the immune system, oncogenesis, and apoptosis. However, the distribution and the function of IRF6 in the central nervous system are limited. In this study, we established an adult rat traumatic brain injury (TBI) model. Compared to the sham brain cortex, Western blot and immunohistochemistry showed significant upregulation of IRF6 in the ipsilateral brain cortex after TBI. Immunofluorescence double-labeling showed that IRF6 completely co-localized with neurons, not astrocytes or oligodendrocytes. Furthermore, we detected that the neuronal apoptosis marker active caspase-3 co-localized with IRF6 in neurons. Additionally, IRF6 knockdown in PC12 cells in vitro resulted in a decrease in active caspase-3 expression and an increase in Bcl-2 and p-Akt expression. We conclude that IRF6 might promote neuronal apoptosis by inhibiting Akt phosphorylation after TBI.
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页码:27 / 36
页数:9
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