Nuclear accumulation of p53 protein following kainic acid‐induced seizures
Nuclear accumulation of p53 protein following kainic acid‐induced seizures
复制标题
红藻氨酸诱导癫痫发作后 p53 蛋白的核积聚
DOI：
10.1097/00001756-199601310-00028
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发表时间：
1996
期刊：
影响因子：
1.7
通讯作者：
S. Schreiber
中科院分区：
文献类型：
--
作者：
S. Sakhi;N. Sun;L. Wing;Parula Mehta;S. Schreiber
p53肿瘤抑制基因与凋亡性细胞死亡有关。本研究旨在探讨p53蛋白表达的增加是否与红藻氨酸诱导的神经元凋亡有关。成年雄性Sprague-Dawley大鼠用谷氨酸盐类似物红藻氨酸进行全身治疗，并在癫痫发作活动开始后4或30小时处死。使用抗p53多克隆抗体在石蜡包埋切片上进行免疫组织化学。在这两个时间点，增加的p53免疫反应性主要在凋亡神经元的细胞核中观察到。这些研究结果提供了额外的支持的假设，即p53是在中枢神经系统中的神经元凋亡的标志物，并表明，核积累的p53蛋白可能是一个重要的介质的神经元死亡。
The p53 tumor suppressor gene has been implicated in apoptotic cell death. The present study was conducted to investigate whether expression of p53 protein is increased in association with kainic acid-induced neuronal apoptosis. Adult male Sprague-Dawley rats were treated systemically with the glutamate analog kainic acid, and sacrificed either 4 or 30 h after the onset of seizure activity. Immunohistochemistry was performed on paraffin-embedded sections using an anti-p53 polyclonal antibody. At both time points, increased p53 immuno-reactivity was observed predominantly in the nucleus of apoptotic neurons. These findings lend additional support to the hypothesis that p53 is a marker of neuronal apoptosis in the CNS, and suggest that nuclear accumulation of p53 protein may be an important mediator of neuronal death.