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

被引:20
作者
Lin, Yuchang [1 ,8 ]
Xu, Dezhi [1 ,8 ]
Li, Xiaohong [2 ,8 ]
Liu, Chun [3 ,8 ]
Liu, Xia [4 ,8 ]
Huang, Shen [5 ,8 ]
Huang, Yuwei [6 ,8 ]
Liu, Xiaojuan [7 ,8 ]
机构
[1] Nanjing Med Univ, Wuxi Hosp 2, Dept Neurosurg, Wuxi 214002, Jiangsu, Peoples R China
[2] Nantong Univ, Affiliated Hosp, Surg Comprehens Lab, Nantong 226001, Jiangsu, Peoples R China
[3] Nantong Univ, Lab Anim Ctr, Nantong 226001, Jiangsu, Peoples R China
[4] Nantong Univ, Dept Pathophysiol, Coll Med, Nantong 226001, Jiangsu, Peoples R China
[5] Nantong Univ, Affiliated Hosp 2, Dept Osteol, Nantong 226001, Peoples R China
[6] Nantong Univ, Inst Nav Med, Nantong 226001, Jiangsu, Peoples R China
[7] Nantong Univ, Dept Pathogen Biol, Coll Med, Nantong 226001, Jiangsu, Peoples R China
[8] Nantong Univ, Coll Med, Jiangsu Prov Key Lab Inflammat & Mol Drug Target, Nantong 226001, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
IRF6; Traumatic brain injury; Neuronal apoptosis; Rat; FACTOR-I; TRANSCRIPTION FACTORS; CASPASE-3; ACTIVATION; REPERFUSION INJURY; ISCHEMIC-STROKE; IRF FAMILY; CELLS; ONCOGENESIS; OVEREXPRESSION; MECHANISMS;
D O I
10.1007/s10571-015-0217-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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.
引用
收藏
页码:27 / 36
页数:10
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