Transgenic mouse overexpressing the Akt reduced the volume of infarct area after middle cerebral artery occlusion
Transgenic mouse overexpressing the Akt reduced the volume of infarct area after middle cerebral artery occlusion
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DOI：
10.1016/j.neulet.2004.02.029
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发表时间：
2004-04-15
影响因子：
2.5
通讯作者：
Kiyama, H
中科院分区：
文献类型：
--
作者：
Ohba, N;Kiryu-Seo, S;Kiyama, H
在损伤诱导神经元内肽酶（DINE）启动子的控制下，用三种不同的小鼠制备了表达活性形式Akt基因的转基因小鼠，并研究了其对缺血性脑损伤的神经保护作用。大脑中动脉闭塞24小时后，两个dine - akt转基因小鼠系显示梗死面积比野生型小鼠减少35%。RT-PCR分析显示，这些细胞系对缺血性脑损伤有高水平的转基因反应。这些结果表明，DINE启动子是一种有用的启动子，它对神经元损伤作出反应，并且akt诱导的神经保护作用在体内对缺血性损伤是有效的。2004爱思唯尔爱尔兰有限公司版权所有。
Transgenic mouse lines expressing the active form Akt gene under the control of the damage-induced neuronal endopeptidase (DINE) promoter were made from three different founder mice, and its neuroprotective potential against ischemic brain damage was investigated. Twenty-four hours after middle cerebral artery occlusion, two DINE-Akt-transgenic mouse lines displayed reductions of the infarcted area by 35% compared to the wild-type littermate. RT-PCR assays showed a high level of transgene in response to ischemic brain damage in these lines. These results suggest that the DINE promoter is a useful promoter, which responds to neuronal insults and that the Akt-induced neuroprotective effect against ischemic damage is potent in vivo. (C) 2004 Elsevier Ireland Ltd. All rights reserved.