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Article

Bioinformatics analysis of gene expression profiles of dermatomyositis

  • Authors:
    • Liang‑Yuan Chen
    • Zhao‑Lei Cui
    • Fan‑Cui Hua
    • Weng‑Jing Yang
    • Ye Bai
    • Feng‑Hua Lan
  • View Affiliations / Copyright

    Affiliations: Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China, Department of Clinical Laboratory, Fujian Provincial Tumor Hospital, Fuzhou, Fujian 350014, P.R. China
  • Pages: 3785-3790
    |
    Published online on: September 2, 2016
       https://doi.org/10.3892/mmr.2016.5703
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Abstract

Dermatomyositis (DM) is a type of autoimmune inflammatory myopathy, which primarily affects the skin and muscle. The underlying mechanisms of DM remain poorly understood. The present study aimed to explore gene expression profile alterations, investigate the underlying mechanisms, and identify novel targets for DM. The GSE48280 dataset, which includes data from five DM and five normal muscle tissue samples, was obtained from the Gene Expression Omnibus. Firstly, differentially expressed genes (DEGs) were screened by limma package in R. Subsequently, functional and pathway enrichment analyses were performed using ClueGO from Cytoscape. Finally, protein‑protein interaction (PPI) networks were constructed using STRING and Cytoscape, in order to identify hub genes. As a result, 180 upregulated and 21 downregulated genes were identified in the DM samples. The Gene Ontology enrichment analysis revealed that the type I interferon (IFN) signaling pathway was the most significantly enriched term within the DEGs. The Kyoto Encyclopedia of Genes and Genomes pathway analysis identified 27 significant pathways, the majority of which can be divided into the infectious diseases and immune system categories. Following construction of PPI networks, 24 hub genes were selected, all of which were associated with the type I IFN signaling pathway in DM. The findings of the present study indicated that type I IFNs may have a central role in the induction of DM. In addition, other DEGs, including chemokine (C‑C motif) ligand 5, C‑X‑C motif chemokine 10, Toll‑like receptor 3, DEXD/H‑Box helicase 58, interferon induced with helicase C domain 1, interferon‑stimulated gene 15 and MX dynamin‑like GTPase 1, may be potential targets for DM diagnosis and treatment.
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Copy and paste a formatted citation
Spandidos Publications style
Chen LY, Cui ZL, Hua FC, Yang WJ, Bai Y and Lan FH: Bioinformatics analysis of gene expression profiles of dermatomyositis. Mol Med Rep 14: 3785-3790, 2016.
APA
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., & Lan, F. (2016). Bioinformatics analysis of gene expression profiles of dermatomyositis. Molecular Medicine Reports, 14, 3785-3790. https://doi.org/10.3892/mmr.2016.5703
MLA
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., Lan, F."Bioinformatics analysis of gene expression profiles of dermatomyositis". Molecular Medicine Reports 14.4 (2016): 3785-3790.
Chicago
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., Lan, F."Bioinformatics analysis of gene expression profiles of dermatomyositis". Molecular Medicine Reports 14, no. 4 (2016): 3785-3790. https://doi.org/10.3892/mmr.2016.5703
Copy and paste a formatted citation
x
Spandidos Publications style
Chen LY, Cui ZL, Hua FC, Yang WJ, Bai Y and Lan FH: Bioinformatics analysis of gene expression profiles of dermatomyositis. Mol Med Rep 14: 3785-3790, 2016.
APA
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., & Lan, F. (2016). Bioinformatics analysis of gene expression profiles of dermatomyositis. Molecular Medicine Reports, 14, 3785-3790. https://doi.org/10.3892/mmr.2016.5703
MLA
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., Lan, F."Bioinformatics analysis of gene expression profiles of dermatomyositis". Molecular Medicine Reports 14.4 (2016): 3785-3790.
Chicago
Chen, L., Cui, Z., Hua, F., Yang, W., Bai, Y., Lan, F."Bioinformatics analysis of gene expression profiles of dermatomyositis". Molecular Medicine Reports 14, no. 4 (2016): 3785-3790. https://doi.org/10.3892/mmr.2016.5703
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