Bioinformatics analysis of gene expression profiles of dermatomyositis.
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.
Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
Liang-Yuan
LY
Chen
Department of Clinical Laboratory, Fujian Provincial Tumor Hospital, Fuzhou, Fujian 350014, P.R. China.
Zhao-Lei
ZL
Cui
Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
Fan-Cui
FC
Hua
Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
Weng-Jing
WJ
Yang
Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
Ye
Y
Bai
Department of Clinical Genetics and Experimental Medicine, Fuzong Clinical School, Fujian Medical University, Fuzhou, Fujian 350025, P.R. China.
Feng-Hua
FH
Lan
D019295:Computational Biology; D003882:Dermatomyositis / Q000235:genetics* / Q000378:metabolism; D020869:Gene Expression Profiling; D063990:Gene Ontology; D053263:Gene Regulatory Networks; D006801:Humans; D010257:Paraneoplastic Syndromes / Q000235:genetics* / Q000378:metabolism; D060066:Protein Interaction Maps; D059467:Transcriptome