Hypoxia/ischemia up-regulates Id2 expression in neuronal cells in vivo and in vitro
Hypoxia/ischemia up-regulates Id2 expression in neuronal cells in vivo and in vitro
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DOI：
10.1016/j.neulet.2013.08.044
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发表时间：
2013-10-25
影响因子：
2.5
通讯作者：
Qiu, Yongming
中科院分区：
文献类型：
--
作者：
Guo, Liemei;Lan, Jin;Qiu, Yongming
DNA结合/分化抑制因子2（Inhibitor of DNA binding/differentiation 2，Id 2）属于转录调节因子家族，其特征在于螺旋-环-螺旋（helix-loop-helix，HLH）基序，缺乏结合DNA所必需的碱性氨基酸结构域。本研究的目的是更好地了解Id 2在缺氧/缺血（H/I）诱导的神经元凋亡中的作用。在大脑中动脉闭塞（MCAO）/再灌注大鼠模型中，H/I诱导后，半暗带区大脑皮质中TUNEL阳性细胞数量逐渐增加，而Id 2 mRNA和蛋白表达也显著上调。模拟缺氧，氯化钴（CoCl 2）处理的大鼠神经母细胞瘤B35细胞系也表现出增强的Id 2 mRNA和蛋白质表达，以及H/I暴露后的亚G1群中的细胞数量增加。Bax蛋白的表达在体内和体外均上调。此外，三重免疫荧光显示Id 2，TUNEL和NeuN在半影区神经元中的明显共定位。提示H/I可上调神经细胞Id 2的表达，Id 2在H/I诱导的神经细胞凋亡中可能起重要作用。(C)2013爱思唯尔爱尔兰有限公司版权所有。
Inhibitor of DNA binding/differentiation 2 (Id2) belongs to a family of transcriptional modulators characterized by a helix-loop-helix (HLH) motif that lacks the basic amino acid domain necessary to bind DNA. The aim of this study was to obtain a better understanding of the role of Id2 in hypoxia/ischemia (H/I)-induced neuronal apoptosis. Following H/I induction in a rat model of middle cerebral artery occlusion (MCAO)/reperfusion, the number of TUNEL-positive cells in cerebral cortices of the penumbra area increased gradually, while the Id2 mRNA and protein expression were also significantly upregulated. The hypoxia-mimetic, cobalt chloride (CoCl2)-treated rat neuroblastoma B35 cell line also demonstrated enhanced Id2 mRNA and protein expression as well as increased number of cells in the sub-G1 populations after H/I exposure. Consistently, the expression of Bax, a proapoptotic protein, was also up-regulated in vivo and in vitro. Moreover, triple immunofluorescence demonstrated the obvious co-localization of Id2, TUNEL and NeuN in neurons of the penumbra area. These data suggest that H/I upregulates Id2 expression in neuronal cells, and Id2 might play an important role in H/I-induced neuronal apoptosis. (C) 2013 Elsevier Ireland Ltd. All rights reserved.