Microarray analysis of long non-coding RNAs in COPD lung tissue
Microarray analysis of long non-coding RNAs in COPD lung tissue
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DOI：
10.1007/s00011-014-0790-9
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发表时间：
2015-02-01
影响因子：
6.7
通讯作者：
Yao, Xin
中科院分区：
文献类型：
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作者：
Bi, Hui;Zhou, Ji;Yao, Xin
长非编码RNA(LncRNAs)在许多人类疾病的发病机制中起着重要作用。在这项研究中，我们描述了没有慢性阻塞性肺疾病(COPD)的非吸烟者、没有COPD的吸烟者和患有COPD的吸烟者的全基因组lncRNA表达。从人肺组织中提取RNA，并使用Agilent Human LncRNA+mRNAArrayv2.0系统进行分析。在所有受试者的肺组织中检测到39,253个不同的lncRNA转录本。在无COPD的吸烟者中，RNA50010|UCSC-9199-1005和RNA58351|CombinedLit_316_550的LncRNAs表达分别最高和最低，与非吸烟者相比，LncRNAs的表达显著上调和下调。与非吸烟者相比，COPD组有120个LncRNAs过度表达，43个LncRNAs低表达，其中RNA44121|UCSC-2000-3182和RNA43510|UCSC-1260-3754分别是最高表达和最低表达。基因本体论(GO)和通路分析表明，吸烟与代谢途径的激活有关，而COPD的转录本与造血细胞谱系、中间代谢和免疫系统过程有关。我们认为，lncRNAs的表达变化可能在COPD的发生和发展中发挥部分作用。
Long noncoding RNAs (lncRNAs) play an important role in the pathogenesis of many human diseases. In this study, we provide the description of genome-wide lncRNA expression in the lung tissue of non-smokers without Chronic obstructive pulmonary disease (COPD), of smokers without COPD and of smokers with COPD.RNA was extracted from human lung tissue and analysed using an Agilent Human lncRNA + mRNA Array v2.0 system.39,253 distinct lncRNA transcripts were detected in the lung tissues of all subjects. In smokers without COPD 87 lncRNAs were significantly up-regulated and 244 down-regulated compared to non-smokers without COPD with RNA50010|UCSC-9199-1005 and RNA58351| CombinedLit_316_550, the most over- and under-regulated, respectively. In contrast, in COPD patients 120 lncRNAs were over-expressed and 43 under-expressed compared with smokers without COPD with RNA44121|UCSC-2000-3182 and RNA43510|UCSC-1260-3754 being the most over- and under-regulated, respectively. Gene Ontology (GO) and pathway analysis indicated that cigarette smoking was associated with activation of metabolic pathways, whereas COPD transcripts were associated with 'hematopoietic cell lineage', intermediary metabolism and immune system processes.We conclude that the altered expression of lncRNAs might play partial role in pathways implicated in COPD onset and progression such as intermediary metabolism and the immune response.