Medical Science Monitor · 2015 · 49 citations · 22 references
Life SciencesBioinformaticsMolecular BiologyGene ExpressionGenomicsTranscriptomicsDifferential Gene Expression AnalysisIntervertebral Disc DiseaseNoncoding Rna BiologyNoncoding Rna TranscriptomicsRna-protein InteractionsTranscriptomic AnalysisGene Ontology EnrichmentIntervertebral Disc DegenerationKegg Pathway EnrichmentMicroarray-based TranscriptomicsNoncoding Rna Differential Expression AnalysisNucleus Pulposus DegenerationProtein-protein Interaction ModulesWeighted Gene Coexpression Network Analysis
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, UBA52 (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, SPHK1 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 UBA52 and SPHK1, may be pivotal biomarkers for IDD.
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