Department of Forensic Medicine and Molecular Pathology, School of Medicine, Kyoto University, Kyoto, Japan.
Dis Model Mech. 2012 Mar;5(2):270-83. doi: 10.1242/dmm.008276. Epub 2011 Oct 20.
Brain ischemia, also termed cerebral ischemia, is a condition in which there is insufficient blood flow to the brain to meet metabolic demand, leading to tissue death (cerebral infarction) due to poor oxygen supply (cerebral hypoxia). Our group is interested in the protective effects of neuropeptides for alleviating brain ischemia, as well as the underlying mechanisms of their action. The present study was initiated to investigate molecular responses at the level of gene expression in ischemic brain tissue. To achieve this, we used a mouse permanent middle cerebral artery occlusion (PMCAO) model in combination with high-throughput DNA microarray analysis on an Agilent microarray platform. Briefly, the right (ipsilateral) and left (contralateral) hemispheres of PMCAO model mice were dissected at two time points, 6 and 24 hours post-ischemia. Total RNA from the ischemic (ipsilateral) hemisphere was subjected to DNA microarray analysis on a mouse whole genome 4x44K DNA chip using a dye-swap approach. Functional categorization using the gene ontology (GO, MGD/AMIGO) of numerous changed genes revealed expression pattern changes in the major categories of cellular process, biological regulation, regulation of biological process, metabolic process and response to stimulus. Reverse-transcriptase PCR (RT-PCR) analysis on randomly selected highly up- or downregulated genes validated, in general, the microarray data. Using two time points for this analysis, major and minor trends in gene expression and/or functions were observed in relation to early- and late-response genes and differentially regulated genes that were further classified into specific pathways or disease states. We also examined the expression of these genes in the contralateral hemisphere, which suggested the presence of bilateral effects and/or differential regulation. This study provides the first ischemia-related transcriptome analysis of the mouse brain, laying a strong foundation for studies designed to elucidate the mechanisms regulating ischemia and to explore the neuroprotective effects of agents such as target neuropeptides.
脑缺血,也称为脑缺血,是指大脑血流灌注不足,无法满足代谢需求,导致组织因供氧不足(脑缺氧)而死亡(脑梗死)。我们小组对神经肽缓解脑缺血的保护作用及其作用机制很感兴趣。本研究旨在研究缺血脑组织中基因表达水平的分子反应。为此,我们使用了一种小鼠永久性大脑中动脉闭塞(PMCAO)模型,并结合安捷伦微阵列平台上的高通量 DNA 微阵列分析。简而言之,在缺血后 6 和 24 小时,从 PMCAO 模型小鼠的右侧(缺血侧)和左侧(对侧)半球中分离出总 RNA。采用染料交换方法,用小鼠全基因组 4x44K DNA 芯片对缺血侧(同侧)半球的总 RNA 进行 DNA 微阵列分析。使用基因本体论(GO、MGD/AMIGO)对大量改变的基因进行功能分类,揭示了主要类别细胞过程、生物调节、生物过程调节、代谢过程和对刺激的反应中的表达模式变化。随机选择高度上调或下调基因的逆转录 PCR(RT-PCR)分析一般验证了微阵列数据。通过对这两个时间点进行分析,观察到与早期和晚期反应基因以及差异调节基因相关的基因表达和/或功能的主要和次要趋势,并进一步将这些基因分类为特定途径或疾病状态。我们还检查了这些基因在对侧半球中的表达情况,这表明存在双侧效应和/或差异调节。本研究提供了小鼠大脑与缺血相关的转录组分析的首次报告,为阐明调节缺血的机制以及探索目标神经肽等药物的神经保护作用奠定了坚实的基础。