Comprehensive Analysis of Transcriptome Sequencing Data in the Lung Tissues of COPD Subjects.

Comprehensive Analysis of Transcriptome Sequencing Data in the Lung Tissues of COPD Subjects.
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DOI:
10.1155/2015/206937
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发表时间:
2015
影响因子:
2.9
通讯作者:
Oh YM
Oh YM
中科院分区:
生物学4区
文献类型:
--
作者:
Kim WJ;Lim JH;Lee JS;Lee SD;Kim JH;Oh YM

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背景和目标。慢性阻塞性肺疾病(COPD)是一种以气流受限为特征的复杂疾病。虽然气道炎症和氧化应激在COPD的发病机制中是重要的,但气流阻塞的机制尚未完全了解。进行肺组织的基因表达谱分析以确定COPD中失调的分子途径。方法.从98例COPD患者和91例肺功能正常的对照者的肺组织中分离RNA。使用HiSeq 2000系统用RNA-seq处理RNA样品。使用Student t检验鉴定两组之间差异表达的基因。结果在过滤了具有零计数的基因和非编码基因之后,评估了16,676个基因。COPD患者和对照组肺组织中共有2312个基因差异表达(校正错误发现率q < 0.01)。COPD患者肺组织中氧化磷酸化和蛋白质降解相关基因表达降低,染色质修饰相关基因表达异常。结论.氧化磷酸化、蛋白质降解和染色质修饰是COPD受试者肺组织中最失调的途径。这些发现可能在COPD中具有临床和机制意义。
Background and Objectives. Chronic obstructive pulmonary disease (COPD) is a complex disease characterized by airflow limitation. Although airway inflammation and oxidative stress are known to be important in the pathogenesis of COPD, the mechanism underlying airflow obstruction is not fully understood. Gene expression profiling of lung tissue was performed to define the molecular pathways that are dysregulated in COPD. Methods. RNA was isolated from lung tissues obtained from 98 subjects with COPD and 91 control subjects with normal spirometry. The RNA samples were processed with RNA-seq using the HiSeq 2000 system. Genes expressed differentially between the two groups were identified using Student's t-test. Results. After filtering for genes with zero counts and noncoding genes, 16,676 genes were evaluated. A total of 2312 genes were differentially expressed between the lung tissues of COPD and control subjects (false discovery rate corrected q < 0.01). The expression of genes related to oxidative phosphorylation and protein catabolism was reduced and genes related to chromatin modification were dysregulated in lung tissues of COPD subjects. Conclusions. Oxidative phosphorylation, protein degradation, and chromatin modification were the most dysregulated pathways in the lung tissues of COPD subjects. These findings may have clinical and mechanistic implications in COPD.
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