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红藻氨酸诱导的兴奋性毒性后丝氨酸58位点14-3-3ζ的磷酸化与神经变性

Phosphorylation of 14-3-3ζ at serine 58 and neurodegeneration following kainic acid-induced excitotoxicity.

作者信息

Jeong Eun Ae, Jeon Byeong Tak, Kim Jeong Bin, Kim Joon Soo, Cho Yong Woon, Lee Dong Hoon, Kim Hyun Joon, Kang Sang Soo, Cho Gyeong Jae, Choi Wan Sung, Roh Gu Seob

机构信息

Department of Anatomy and Neurobiology, Institute of Health Sciences, Medical Research Center for Neural Dysfunction, Biomedical Center (BK21), Gyeongsang National University School of Medicine, Jinju, Korea.

出版信息

Anat Cell Biol. 2010 Jun;43(2):150-6. doi: 10.5115/acb.2010.43.2.150. Epub 2010 Jun 30.

Abstract

Oxidative stress-induced cell death leads to phosphorylation of 14-3-3ζ at serine 58. 14-3-3ζ is detected at significant levels in cerebrospinal fluid after kainic acid (KA)-induced seizures. Here we examined temporal changes in 14-3-3ζ phosphorylation in the hippocampus and amygdala of mice after KA treatment. Mice were killed at 2, 6, 24, or 48 h after KA (30 mg/kg) injection. We observed an increase in TUNEL and Fluoro-Jade B (FJB)-stained neurons in the hippocampus and amygdala of KA-treated mice. Phospho (p)-14-3-3ζ and p-JNK expression was increased in the hippocampus 2 and 6 h after KA treatment, respectively. In immunohistochemical analysis, p-14-3-3ζ-positive cells were present in the CA3 region of the hippocampus and the central nucleus of amygdala (CeA) of KA-treated mice. Thus, phosphorylation of 14-3-3ζ at serine 58 may play an important role in KA-induced hippocampal and amygdaloid neuronal damage.

摘要

氧化应激诱导的细胞死亡导致14-3-3ζ丝氨酸58位点磷酸化。在 kainic 酸(KA)诱导癫痫发作后,脑脊液中可检测到显著水平的14-3-3ζ。在此,我们研究了KA处理后小鼠海马体和杏仁核中14-3-3ζ磷酸化的时间变化。在注射KA(30mg/kg)后2、6、24或48小时处死小鼠。我们观察到KA处理小鼠的海马体和杏仁核中TUNEL和Fluoro-Jade B(FJB)染色神经元增加。KA处理后2小时和6小时,海马体中磷酸化(p)-l4-3-3ζ和p-JNK表达分别增加。在免疫组织化学分析中,KA处理小鼠的海马体CA3区和杏仁核中央核(CeA)中存在p-14-3-3ζ阳性细胞。因此,14-3-3ζ丝氨酸58位点的磷酸化可能在KA诱导的海马体和杏仁核神经元损伤中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a5/2998790/bc3cbdad823c/acb-43-150-g001.jpg

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