Wu Tao, Wu Huan-Dong, Xu Zao-Xian, Han Fei, Zhang Bi-Qi, Sun Jian, Hu Shen-Jiang
Hangzhou JunKangYiDe Hospital, No.26 North Xueyuan Road, Hangzhou, 310011, Zhejiang Province, People's Republic of China.
Department of Cardiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, No. 79, Qingchun Road, ShangCheng District, Hangzhou, 310003, Zhejiang Province, People's Republic of China.
Heart Vessels. 2017 Oct;32(10):1253-1261. doi: 10.1007/s00380-017-0990-7. Epub 2017 May 23.
Myocardial infarction (MI) is the leading cause of fatality worldwide. Our study aimed to investigate the dysregulated long non-coding RNA (lncRNA) in MI and elucidate the mechanism of it in MI. The lncRNA and mRNA expression profiling of the whole left ventricular tissue of MI mice model (8 mice) and Sham group (8 mice) was obtained based on microarray analysis. Differentially expressed lnRNAs/mRNA (DELs/DEMs) were identified in MI. DELs/DEMs co-expression network construction, gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were conducted to predict the biological functions of DEMs. Quantitative real-time polymerase chain reaction (qRT-PCR) was subjected to validate the abnormally expressed DELs in left ventricular tissues of MI mice model. Total of 168 DELs (37 up- and 131 down-regulated) and 126 DEMs (87 up- and 39 down-regulated) were identified in MI compared with Sham group. The co-expression network of candidate DELs and DEMs was constructed, which covered 219 nodes and 1775 edges. The qRT-PCR validation results indicated that ENSMUST00000124047 was significantly down-regulated in MI group and AK166279 was significantly up-regulated in MI group. ENSMUST00000121611 and NR_015515 had the up-regulated tendency in MI group compared with Sham group. The DEMs in MI were significantly enriched in 41 signaling pathways including complement and coagulation cascades, cytokine-cytokine receptor interaction and chemokine signaling pathway. The expression profiling of dysregulated DELs in MI was identified. Our results might provide useful information for exploring the pathogenesis mechanism of MI.
心肌梗死（MI）是全球范围内致死的主要原因。我们的研究旨在调查MI中失调的长链非编码RNA（lncRNA），并阐明其在MI中的作用机制。基于微阵列分析，获得了MI小鼠模型（8只小鼠）和假手术组（8只小鼠）整个左心室组织的lncRNA和mRNA表达谱。在MI中鉴定出差异表达的lnRNA/mRNA（DELs/DEMs）。进行DELs/DEMs共表达网络构建、基因本体（GO）和京都基因与基因组百科全书（KEGG）富集分析，以预测DEMs的生物学功能。采用定量实时聚合酶链反应（qRT-PCR）验证MI小鼠模型左心室组织中异常表达的DELs。与假手术组相比，MI中总共鉴定出168个DELs（37个上调和131个下调）和126个DEMs（87个上调和39个下调）。构建了候选DELs和DEMs的共表达网络，该网络涵盖219个节点和1775条边。qRT-PCR验证结果表明，ENSMUST00000124047在MI组中显著下调，AK166279在MI组中显著上调。与假手术组相比，ENSMUST00000121611和NR_015515在MI组中有上调趋势。MI中的DEMs在41条信号通路中显著富集，包括补体和凝血级联反应、细胞因子-细胞因子受体相互作用和趋化因子信号通路。鉴定了MI中失调的DELs的表达谱。我们的结果可能为探索MI的发病机制提供有用信息。
