Heart Center, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Biomed Res Int. 2019 Jul 4;2019:3945475. doi: 10.1155/2019/3945475. eCollection 2019.
The expression profile of long noncoding RNA (lncRNA) in human epicardial adipose tissue (EAT) has not been widely studied. In the present study, we performed RNA sequencing to analyze the expression profiles of lncRNA and mRNA in EAT in coronary artery disease (CAD) patients with and without heart failure (HF). Our results showed RNA sequencing disclosed 35673 mRNA and 11087 lncRNA corresponding to 15554 genes in EAT in total, while 30 differentially expressed lncRNAs (17 upregulated and 13 downregulated) and 278 differentially expressed mRNAs (129 upregulated and 149 downregulated) were discriminated between CAD patients with and without HF (<0.05; fold change>2); lncRNA ENST00000610659 drew specific attention for it was the top upregulated lncRNA with highest fold change and corresponded to UNC93B1 gene, which was proved to be related to HF and encoded UNC93B1 protein regulating toll-like receptor signaling, and both of them significantly increased in HF patients in qRT-PCR validation; the top significant upregulated enriched GO terms and KEGG pathway analysis were regulation of lymphocyte activation (GO:0051249) and T cell receptor signaling pathway (hsa04660), respectively. The current findings support the fact that EAT lncRNAs are involved in the inflammatory response leading to the development of HF.
人类心外膜脂肪组织（EAT）中长链非编码 RNA（lncRNA）的表达谱尚未得到广泛研究。在本研究中，我们进行了 RNA 测序，以分析冠心病（CAD）伴或不伴心力衰竭（HF）患者 EAT 中 lncRNA 和 mRNA 的表达谱。我们的结果显示，RNA 测序共揭示了 EAT 中 35673 个 mRNA 和 11087 个 lncRNA，对应 15554 个基因，而 CAD 伴或不伴 HF 患者之间有 30 个差异表达的 lncRNA（17 个上调和 13 个下调）和 278 个差异表达的 mRNA（129 个上调和 149 个下调）（<0.05；倍数变化>2）；lncRNA ENST00000610659 引起了特别关注，因为它是上调倍数最高的 top 上调 lncRNA，对应 UNC93B1 基因，该基因被证明与 HF 有关，并编码 UNC93B1 蛋白，调节 Toll 样受体信号，两者在 qRT-PCR 验证中均在 HF 患者中显著增加；top 显著上调的富集 GO 术语和 KEGG 通路分析分别为淋巴细胞激活的调节（GO:0051249）和 T 细胞受体信号通路（hsa04660）。目前的研究结果支持这样一个事实，即 EAT lncRNA 参与了导致 HF 发展的炎症反应。
