机构：[1]Clinical Medical College of Yangzhou University, Yangzhou, Jiangsu Province, China[2]Department of Neurology, Northern Jiangsu People’s Hospital, Yangzhou, Jiangsu Province, China[3]Institute of Neuroscience, Northern Jiangsu People’s Hospital, Yangzhou, Jiangsu Province, China[4]Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu Province, China[5]Dalian Medical University, Dalian, Liaoning Province, China[6]Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China
Epithelial-specific ETS-1 (ESE1), a member of the ETS transcription factor family, is widely expressed in multiple tissues and performs various functions in inflammation. During neuroinflammation, ESE1 promotes neuronal apoptosis; however, the expression and biological functions of ESE1 remain unclear after cerebral ischemia/reperfusion. We performed in vivo and in vitro experiments to explore the role of ESE1 in cerebral ischemic injury. A modified four vessel occlusion method was used in adult Sprague-Dawley rats. At 6, 12, 24, 48, and 72 hours after model induction, the hippocampus was collected for analysis. Western blot assays and immunohistochemistry showed that the expression of ESE1, phosphorylated p65 and active caspase-3 was significantly up-regulated after ischemia. Double hnmunofluo-rescence staining indicated that ESE1 and NeuN were mostly co-located in the hippocampus after ischemia. Furthermore, ESE1 was also co-expressed with active caspase-3. PC12 cells were stimulated with cobalt chloride (CoCl2) to establish a chemical hypoxia model. After ESE1 knockdown by siRNA for 6 hours, cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assays. The levels of ESE1, phosphorylated p65 and active caspase-3 were also remarkably increased in PC12 cells after CoCl2 stimulation. After ESE1 knockdown, PC12 cell viability was increased after hypoxia. siRNA knockdown of ESE1 decreased the level of p-p65 and active caspase-3 after CoCl2 stimulation. These data reveal that ESE1 levels are elevated in the hippocampus after cerebral ischemia/reperfusion injury. This may play a role in neuronal apoptosis via activation of the nuclear factor-kappa B pathway.
基金：
National Natural Science Foundation of China [81400963]; 333 Project of Jiangsu Province of China [BRA2015187]; Medical Youth Talent Foundation of Jiangsu Province of China [QNRC2016327, QNRC2016328, QNRC2016326]
第一作者机构：[1]Clinical Medical College of Yangzhou University, Yangzhou, Jiangsu Province, China[2]Department of Neurology, Northern Jiangsu People’s Hospital, Yangzhou, Jiangsu Province, China[3]Institute of Neuroscience, Northern Jiangsu People’s Hospital, Yangzhou, Jiangsu Province, China[4]Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu Province, China
共同第一作者：
通讯作者：
通讯机构：[1]Clinical Medical College of Yangzhou University, Yangzhou, Jiangsu Province, China[2]Department of Neurology, Northern Jiangsu People’s Hospital, Yangzhou, Jiangsu Province, China[6]Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China
推荐引用方式(GB/T 7714)：
Yu Hai-Long,Wang Liang-Zhu,Zhang Ling-Ling,et al.ESE1 expression correlates with neuronal apoptosis in the hippocampus after cerebral ischemia/reperfusion injury[J].NEURAL REGENERATION RESEARCH.2019,14(5):841-849.doi:10.4103/1673-5374.249232.
APA：
Yu, Hai-Long,Wang, Liang-Zhu,Zhang, Ling-Ling,Chen, Bei-Lei,Zhang, Hui-Juan...&Chen, Ying-Zhu.(2019).ESE1 expression correlates with neuronal apoptosis in the hippocampus after cerebral ischemia/reperfusion injury.NEURAL REGENERATION RESEARCH,14,(5)
MLA：
Yu, Hai-Long,et al."ESE1 expression correlates with neuronal apoptosis in the hippocampus after cerebral ischemia/reperfusion injury".NEURAL REGENERATION RESEARCH 14..5(2019):841-849
