Up-regulation of FOS-like antigen 1 contributes to neuronal apoptosis in the cortex of rat following traumatic brain injury
Up-regulation of FOS-like antigen 1 contributes to neuronal apoptosis in the cortex of rat following traumatic brain injury
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FOS样抗原1的上调有助于大鼠脑外伤后皮质中的神经元凋亡
DOI：
10.1007/s11011-017-0129-7
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发表时间：
2018-02
期刊：
影响因子：
--
通讯作者：
Qing Lan
中科院分区：
文献类型：
--
作者：
Xide Xu;Rui Jiang;Peipei Gong;Qianqian Liu;Yinan Chen;Shiqiang Hou;Debin Yuan;Jiansheng Shi;Qing Lan
神经细胞凋亡是颅脑损伤后继发性脑损伤的一个重要过程，是由神经化学信号转导引起的。本研究旨在探讨FOS样抗原1(Fra-1)是否参与神经细胞的凋亡。免疫组织化学和Western印迹分析显示，在大鼠脑损伤模型中，同侧大脑皮质中Fra-1的表达显著增加，与活性caspase-3的表达增加相平行。免疫荧光双标记法将Fra-1与活化的caspase-3和神经元标记物Neun共定位。在体外细胞损伤模型中，过氧化氢可诱导细胞凋亡，降低细胞存活率，同时PC12细胞中caspase-3、P53和Fra-1的表达也有类似的增加。通过转染Fra-1 siRNA下调Fra-1的表达可显著提高PC12细胞的存活率，降低活化的caspase-3和P53的表达，减少H_2O_2作用后PC12细胞的凋亡率。综上所述，本研究结果提示，Fra-1可能通过上调P53信号通路参与诱导神经细胞凋亡，这一作用可能参与了脑外伤后的继发性神经病理过程。
Neuronal apoptosis is an important process of secondary brain injury which is induced by neurochemical signaling cascades after traumatic brain injury (TBI). Present study was designed to investigate whether FOS-like antigen 1 (Fra-1) is involved in the neuronal apoptosis. Western blot analysis and immunohistochemistry in a rat TBI model revealed a significant increase in the expression of Fra-1 in the ipsilateral brain cortex, which was in parallel with increase in the expression of active caspase-3. With immunofluorescence double-labeling, Fra-1 was colocalized with active caspase-3 and with NeuN, a neuronal marker. In an in vitro cell injury model, H2O2exposure induced cell apoptosis and reduced cell viability and at the same time, a similar increased expression of active caspase-3, p53 and Fra-1 was found in PC12 cells. Down-regulation of Fra-1 through transfection with Fra-1 siRNA remarkably elevated cell viability, reduced the expression of active caspase-3 and p53, and decreased apoptosis of PC12 cells after H2O2exposure. Taken together, present findings suggest that Fra-1 may be involved in the induction of neuronal apoptosis through up-regulating p53 signaling pathway and that this action may contribute to the secondary neuropathological process after TBI.
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影响因子：
2.9
作者：
E. Pozas;F. Aguado;I. Ferrer
通讯作者：
E. Pozas;F. Aguado;I. Ferrer
选择性 CDK 抑制剂：未来临床创伤性脑损伤试验的有希望的候选者。
影响因子：
6.1
作者：
Kabadi SV;Faden AI
通讯作者：
Faden AI
影响因子：
7.2
作者：
Yuan, Junying
通讯作者：
Yuan, Junying
DOI：
10.1016/0169-328x(96)00059-9
发表时间：
1996-09-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
Gillardon, F;Lenz, C;Kuschinsky, W
通讯作者：
Kuschinsky, W
Fra-1参与大鼠光致视网膜损伤模型视网膜神经节细胞凋亡
影响因子：
4
作者：
Liu, Xiaojuan;Yang, Xiaowei;Chen, Hui
通讯作者：
Chen, Hui