Differential gene expression in the rat cochlea after exposure to impulse noise
Differential gene expression in the rat cochlea after exposure to impulse noise
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DOI：
10.1016/j.neuroscience.2006.06.037
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发表时间：
2006-10-13
期刊：
影响因子：
3.3
通讯作者：
Ulfendahl, M.
中科院分区：
文献类型：
--
作者：
Kirkegaard, M.;Murai, N.;Ulfendahl, M.
了解噪声损伤的分子生物学对于制定有效和及时的干预措施至关重要。在爆炸介导的脉冲噪声损伤模型中，在暴露后3和24小时，在整个大鼠耳蜗制备的差异基因表达进行了研究。我们开发了一种技术，在每个寡核苷酸微阵列上使用来自单个耳蜗的mRNA，以避免合并mRNA样品。保守的统计分析方法的应用导致61个差异表达基因的鉴定。暴露后3 h内，即刻早期基因表达上调，主要是转录因子和参与组织对氧化应激反应的基因。没有发现基因被显著下调。在暴露后24小时，上调的基因包括炎症和抗氧化途径的成员和一个参与谷胱甘肽代谢的基因下调。通过实时逆转录-聚合酶链反应（RT-PCR）确认基因的子集。本研究证明了微阵列技术在提供噪声暴露后的基因调控的全局视图中的能力，并在识别可能在听力损失中具有重要机械作用的基因中，从而作为开发治疗干预措施的基础。(c)2006年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Understanding the molecular biology of noise trauma is vital to developing effective and timely interventions. In a model of explosion-mediated impulse noise injury, differential gene expression was studied in whole rat cochlea preparations at 3 and 24 h following the exposure. We developed a technique using mRNA from a single cochlea on each oligonucleotide microarray to avoid pooling of mRNA samples. Application of a conservative statistical analysis approach resulted in the identification of 61 differentially expressed genes. Within 3 h after the exposure, there was an up-regulation of immediate early genes, mainly transcription factors and genes involved in the tissue's response to oxidative stress. No genes were found to be significantly down-regulated. At 24 h following the exposure, up-regulated genes included members of inflammatory and antioxidant pathways and one gene involved in glutathione metabolism was down-regulated. A subset of genes was confirmed by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). The present study demonstrates the power of the microarray technique in providing a global view of the gene regulation following noise exposure, and in identifying genes that may be mechanistically important in hearing loss, and thereby serve as a basis for the development of therapeutic interventions. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved.