Abstract
AbstractBackgroundDermatomyositis (DM) is an idiopathic inflammatory myopathy (IIM). In this study, we investigated the mRNAs and long noncoding RNAs (lncRNAs) in muscle biopsy specimens that are differentially expressed among patients with DM, patients with other IIM, and healthy controls (HCs).MethodsIn total, three patients with DM, 10 patients with other IIM, and three HCs were included. Muscle biopsy specimens were collected for RNA‐sequencing. Gene ontology and pathway analyses were employed to characterize the biological processes and signaling pathways.ResultsCompared with HCs, 372 differentially expressed mRNAs were identified within the DM group, including 275 upregulated and 97 downregulated ones. Moreover, 692 differentially expressed lncRNAs were identified in the DM group compared with HCs, of which 407 were upregulated and 285 were downregulated. Bioinformatic analysis indicated that the type‐I interferon signaling pathway and biological processes of innate immunity were significantly influenced by the differentially expressed mRNAs. Notably, 11 of the top 20 upregulated mRNAs were involved in the type‐I interferon signaling pathway. Reverse transcription polymerase chain reaction analysis verified the RNA‐sequencing data. Target gene prediction analysis suggested that the lncRNA NONHSAG043573.2 potentially targeting transporter associated with antigen processing 1, a key regulator of interferon signaling genes, might play an important role in the pathogenesis of DM.ConclusionsOur study assessed the transcriptomic profiles of differentially expressed mRNAs and lncRNAs in the DM muscle tissue and revealed that the upregulated mRNAs are significantly involved in the innate immune response and the type‐I interferon signaling pathway, which might play important roles in the pathogenesis of DM.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.