Abstract
Objective The aim of this study is to explore the potential pathogenesis of juvenile dermatomyositis by bioinformatics analysis of gene chips, which would screen the hub genes, identify potential biomarkers, and reveal the development mechanism of juvenile dermatomyositis. Material and Methods We retrieved juvenile dermatomyositis's original expression microarray data of message RNAs (mRNAs) and microRNAs (miRNAs) from NCBI's Gene Expression Omnibus database (GEO, http://www.ncbi.nlm.nih.gov/geo/); through the R package of limma in Bioconductor, we can screen the differentially expressed miRNAs and mRNAs, and then we further analyzed the predicted target genes by the methods such as Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and miRNA-mRNA regulatory network construction and protein-protein interaction (PPI) network using Cytoscape 3.6.1. Results Compared with normal juvenile skin tissues, 6 upregulated microRNAs and 5 downregulated microRNAs were identified from 166 downregulated microRNAs and 58 upregulated microRNAs in juvenile dermatomyositis tissues. The enrichment pathways of differentially expressed microRNAs include cell adhesion molecules (CAMs), autoimmune thyroid disease, Type I diabetes mellitus, antigen and presentation, viral myocardium, graft-versus-host disease, and Kaposi sarcoma-associated herpes virus infection. By screening of microRNA-messenger RNA regulatory network and construction of PPI network map, three target miRNAs were identified, namely, miR-193b, miR-199b-5p, and miR-665. Conclusion We identified mir-193b, mir-199b-5p, and mir-6653 target miRNAs by exploring the miRNA-mRNA regulation network mechanism related to the pathogenesis of juvenile dermatomyositis, which will be of great significance for further study on the pathogenesis and targeted therapy of juvenile dermatomyositis.
Highlights
Juvenile dermatomyositis (JDM) is a chronic autoimmune connective tissue disease
The computational analysis predicts that miRNAs regulate about 30% of all human genes, and the miRNAmRNA regulatory network regulates a variety of biological pathways and processes through complex relationships [9]
JDM is an autoimmune connective tissue disease with immunological abnormalities and positive autoantibodies. It has intricate clinical manifestations, so that it is sometimes difficult to cure that [10, 11]. erefore, if not detected and not treated early in time, JDM would lead to poor prognosis and seriously reduce the quality of life of patients, or even endanger the lives of patients [12,13,14,15]
Summary
Juvenile dermatomyositis (JDM) is a chronic autoimmune connective tissue disease. Its clinical manifestation is inflammatory myopathy with characteristic skin lesions, like Gottron’s papules and heliotrope rash [1,2,3,4]. e incidence of JDM is about 1.9–4.1/1,000,000 [5]. e pathogenesis in juvenile is not clear yet, the clinical manifestations of JDM are complex, and its serious cases can even worsen and significantly impact on the prognosis, for example, unspecific clinical course, risk of macrophage activation syndrome, and more in general, chronic systemic inflammation [6, 7]. erefore, it is urgent to find new diagnostic ideas and new therapies for JDM.More and more literature indicate that miRNAs play a major role in the occurrence, development, and prognosis of inflammatory myopathy [8]. e latest studies using highthroughput microarray to analyze samples from JDM patients and normal juveniles have given us the opportunity to detect and explore different levels of JDM from genome copy number changes and somatic mutations to transcription levels of gene expression changes and discover the entire molecular landscape of inflammation. Juvenile dermatomyositis (JDM) is a chronic autoimmune connective tissue disease. E pathogenesis in juvenile is not clear yet, the clinical manifestations of JDM are complex, and its serious cases can even worsen and significantly impact on the prognosis, for example, unspecific clinical course, risk of macrophage activation syndrome, and more in general, chronic systemic inflammation [6, 7]. E latest studies using highthroughput microarray to analyze samples from JDM patients and normal juveniles have given us the opportunity to detect and explore different levels of JDM from genome copy number changes and somatic mutations to transcription levels of gene expression changes and discover the entire molecular landscape of inflammation. There have been previous studies involving miRNA-mRNA analysis of JDM, in our knowledge, the regulatory network of miRNAs in JDM has not been constructed.
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