急性缺血性脑损伤基因表达谱的计算模型

J. Kola, K. Revett
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引用次数: 0

摘要

脑缺血后的后续事件是复杂和多方面的,因此很难提取缺血期间改变的各种途径之间的因果关系。在这项研究中,我们分析了急性实验性缺血性中风的全面DNA微阵列数据集,试图阐明参与触发导致组织损伤的途径的关键调控元件。数据表明,负责即时早期基因、细胞凋亡、神经递质受体(主要是谷氨酸)和炎症的基因在实验性缺血后的不同时间点上表达差异。利用无监督聚类(自组织图)和基因调控网络,我们能够建立一个框架,在其中我们可以放置最终的基因表达变化。虽然尚未完成,但这项研究的结果表明,即使是像缺血这样复杂的病理,也可以使用DNA微阵列技术以生物学上有意义的方式进行分析
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Computational modelling of the gene expression profile from acute ischaemic brain injury
The ensuing events subsequent to cerebral ischaemia are complex and multi-faceted, making it difficult to extract causal relationships between the various pathways that are altered during ischaemia. In this study, we analyse a comprehensive DNA microarray dataset of acute experimental ischaemic stroke, in an effort to elucidate key regulatory elements that participate in the triggering of the pathways that lead to tissue damage. The data suggest that genes responsible for immediate early genes, apoptosis, neurotransmitter receptors (principally glutamate), and inflammation are differentially expressed at various time points subsequent to experimental ischaemia. Using unsupervised clustering (self-organising maps) and gene regulatory networks, we were able to establish a framework within which we could place the resultant gene expression changes into. Although not yet complete, the results from this study indicate that even a complicated pathology such as ischaemia can be analysed in a biologically meaningful way using DNA microarray technology
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