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Potential Role of lncRNAs in Contributing to Pathogenesis of Intervertebral Disc Degeneration Based on Microarray Data

机译:基于微阵列数据的lncRNAs在椎间盘退变发病机理中的潜在作用

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BACKGROUND Our study intended to identify potential long non-coding RNAs (lncRNAs) and genes, and to elucidate the underlying mechanisms of intervertebral disc degeneration (IDD). MATERIAL AND METHODS The microarray of GSE56081 was downloaded from the Gene Expression Omnibus database, including 5 human control nucleus pulposus tissues and 5 degenerative nucleus pulposus tissues, which was on the basis of GPL15314 platform. Identification of differentially expressed lncRNAs and mRNAs were performed between the 2 groups. Then, gene ontology (GO) and pathway enrichment analyses were performed to analyze the biological functions and pathways for the differentially expressed mRNAs. Simultaneously, lncRNA-mRNA weighted coexpression network was constructed using the WGCNA package, followed by GO and KEGG pathway enrichment analyses for the genes in the modules. Finally, the protein-protein interaction (PPI) network was visualized. RESULTS A total of 135 significantly up- and 170 down-regulated lncRNAs and 2133 significantly up- and 1098 down-regulated mRNAs were identified. Additionally, [i]UBA52[/i] (ubiquitin A-52 residue ribosomal protein fusion product 1), with the highest connectivity degree in PPI network, was remarkably enriched in the pathway of metabolism of proteins. Eight lncRNAs – LINC00917, CTD-2246P4.1, CTC-523E23.5, RP4-639J15.1, RP11-363G2.4, AC005082.12, MIR132, and RP11-38F22.1 – were observed in the modules of lncRNA-mRNA weighted coexpression network. Moreover, [i]SPHK1[/i] in the green-yellow module was significantly enriched in positive regulation of cell migration. CONCLUSIONS LncRNAs LINC00917, CTD-2246P4.1, CTC-523E23.5, RP4-639J15.1, RP11-363G2.4, AC005082.12, MIR132, and RP11-38F22.1 were differentially expressed and might play important roles in the development of IDD. Key genes, such as [i]UBA52[/i] and [i]SPHK1[/i], may be pivotal biomarkers for IDD.
机译:背景技术我们的研究旨在鉴定潜在的长非编码RNA(lncRNA)和基因,并阐明椎间盘退变(IDD)的潜在机制。材料与方法GSE56081的微阵列是从Gene Expression Omnibus数据库下载的,其中包括5个基于GPL15314平台的人类控制髓核组织和5个变性髓核组织。在两组之间鉴定差异表达的lncRNA和mRNA。然后,进行基因本体论(GO)和途径富集分析,以分析差异表达mRNA的生物学功能和途径。同时,使用WGCNA软件包构建了lncRNA-mRNA加权共表达网络,然后对模块中的基因进行了GO和KEGG途径富集分析。最后,可视化了蛋白质-蛋白质相互作用(PPI)网络。结果共鉴定出135个显着上调的lncRNA和170个下调的lncRNA,以及2133个上调和1098个显着下调的mRNA。此外,在PPI网络中具有最高连接度的[i] UBA52 [/ i](泛素A-52残基核糖体蛋白融合产物)显着丰富了蛋白质的代谢途径。在lncRNA-的模块中观察到八个lncRNA-LINC00917,CTD-2246P4.1,CTC-523E23.5,RP4-639J15.1,RP11-363G2.4,AC005082.12,MIR132和RP11-38F22.1 mRNA加权共表达网络。此外,绿黄色模块中的[i] SPHK1 [/ i]显着丰富了细胞迁移的正向调控。结论LncRNA LINC00917,CTD-2246P4.1,CTC-523E23.5,RP4-639J15.1,RP11-363G2.4,AC005082.12,MIR132和RP11-38F22.1差异表达且可能在其中起重要作用开发IDD。关键基因,例如[i] UBA52 [/ i]和[i] SPHK1 [/ i],可能是IDD的关键生物标志物。

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