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大鼠早期氧诱导视网膜病变的基因表达微阵列分析

Gene expression microarray analysis of early oxygen-induced retinopathy in the rat.

作者信息

Tea Melinda, Fogarty Rhys, Brereton Helen M, Michael Michael Z, Van der Hoek Mark B, Tsykin Anna, Coster Douglas J, Williams Keryn A

出版信息

J Ocul Biol Dis Infor. 2009 Dec 12;2(4):190-201. doi: 10.1007/s12177-009-9041-7.

Abstract

Different inbred strains of rat differ in their susceptibility to oxygen-induced retinopathy (OIR), an animal model of human retinopathy of prematurity. We examined gene expression in Sprague-Dawley (susceptible) and Fischer 344 (resistant) neonatal rats after 3 days exposure to cyclic hyperoxia or room air, using Affymetrix rat Genearrays. False discovery rate analysis was used to identify differentially regulated genes. Such genes were then ranked by fold change and submitted to the online database, DAVID. The Sprague-Dawley list returned the term "response to hypoxia," absent from the Fischer 344 output. Manual analysis indicated that many genes known to be upregulated by hypoxia-inducible factor-1alpha were downregulated by cyclic hyperoxia. Quantitative real-time RT-PCR analysis of Egln3, Bnip3, Slc16a3, and Hk2 confirmed the microarray results. We conclude that combined methodologies are required for adequate dissection of the pathophysiology of strain susceptibility to OIR in the rat. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s12177-009-9041-7) contains supplementary material, which is available to authorized users.

摘要

不同的近交系大鼠对氧诱导性视网膜病变(OIR)的易感性存在差异,OIR是一种人类早产儿视网膜病变的动物模型。我们使用Affymetrix大鼠基因芯片,检测了暴露于周期性高氧或室内空气3天后的Sprague-Dawley(易感)和Fischer 344(抗性)新生大鼠的基因表达。采用错误发现率分析来识别差异调节基因。然后根据倍数变化对这些基因进行排序,并提交到在线数据库DAVID。Sprague-Dawley列表返回了“对缺氧的反应”这一术语,而Fischer 344的输出中没有该术语。人工分析表明,许多已知由缺氧诱导因子-1α上调的基因在周期性高氧作用下被下调。对Egln3、Bnip3、Slc16a3和Hk2进行定量实时RT-PCR分析,证实了芯片结果。我们得出结论,需要综合多种方法来充分剖析大鼠对OIR品系易感性的病理生理学机制。电子补充材料:本文的在线版本(doi:10.1007/s12177-009-9041-7)包含补充材料,授权用户可获取。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e63/2839845/b4153675b7f9/12177_2009_9041_Fig1_HTML.jpg

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