The synchronized gene expression of retrotransposons and type I interferon in dermatomyositis

Kuriyama, Yuko; Shimizu, Akira; Kanai, Saki; Oikawa, Daisuke; Tokunaga, Fuminori; Tsukagoshi, Hiroyuki; Ishikawa, Osamu

doi:10.1016/j.jaad.2020.05.051

Cited by 4 publications

(3 citation statements)

References 5 publications

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“…To understand the functions of these DEGs between the DM and healthy control groups, we conducted a functional enrichment analysis that revealed these DEGs play significant roles in various functions, including the type I interferon signaling pathway, cytokine activity, chemokine activity, CCR chemokine receptor binding, double-stranded RNA binding, and blood microparticles. Several previous studies have confirmed our finding that the type I interferon signaling pathway plays a critical role in DM (16)(17)(18)(19)(20). Baechler et al revealed that increased expression levels of type I interferon signatures are associated with DM (17).…”

Section: Discussionsupporting

confidence: 90%

Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis

Wang¹,

Fang²,

Liu³

2022

Ann Transl Med

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Section: Discussionsupporting

confidence: 90%

Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis

Wang¹,

Fang²,

Liu³

2022

Ann Transl Med

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“…1 D and 2 ). Our results suggested that the altered expression of retrotransposons may induce constitutive type I IFN signaling prematurely, and additional factors, such as viral infections, may further upregulate the type I IFN pathway 32 , leading to the development of autoimmune diseases. In contrast, type II IFN activation was not correlated with retrotransposon expression (Figs.…”

Section: Discussionmentioning

confidence: 82%

“…We extracted RNA from peripheral blood cells from patients receiving treatment. The DM and healthy control samples (HC) were the same as those described previously 32 . We also collected biopsied skin samples from the lesions (erythema, vesicle and erosion) of 11 SLE patients, 9 AIBD patients, 3 DM patients, and 3 healthy individuals.…”

Section: Methodsmentioning

confidence: 99%

Coordination of retrotransposons and type I interferon with distinct interferon pathways in dermatomyositis, systemic lupus erythematosus and autoimmune blistering disease

Kuriyama

Shimizu

Kanai

et al. 2021

Sci Rep

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Type I interferon (IFN) plays a crucial role in innate and adaptive immunity, and aberrant IFN responses are involved in systemic autoimmune diseases, such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Type I IFNs can be induced by transcribed retrotransposons. The regulation of retrotransposons and type I IFN and the downstream IFN pathways in SLE, DM, and autoimmune blistering disease (AIBD) were investigated. The gene expression levels of retrotransposons, including LINE-1, type I-III IFNs, and IFN-stimulated genes (ISGs) in peripheral blood cells from patients with DM (n = 24), SLE (n = 19), AIBD (n = 14) and healthy controls (HCs, n = 10) were assessed by quantitative polymerase chain reaction. Upregulation of retrotransposons and IFNs was detected in DM patient samples, as is characteristic, compared to HCs; however, ISGs were not uniformly upregulated. In contrast, retrotransposons and IFNs, except for type II IFN, such as IFN-γ, were not upregulated in SLE. In AIBD, only some retrotransposons and type I interferons were upregulated. The DM, SLE, and AIBD samples showed coordinated expression of retrotransposons and type I IFNs and distinct spectra of IFN signaling. A positive correlation between LINE-1 and IFN-β1 was also detected in human cell lines. These factors may participate in the development of these autoimmune diseases.

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IFN-beta and EIF2AK2 are potential biomarkers for interstitial lung disease in anti-MDA5 positive dermatomyositis

et al. 2023

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Objective Dermatomyositis (DM) with positive anti-melanoma differentiation-related gene 5 (MDA5) antibody is an autoimmune disease with multiple complications. Interstitial lung diseases (ILD) are significantly associated with DM and are particularly related to MDA5+ DM. This article aimed to explore potential molecular mechanisms and develop new diagnostic biomarkers for MDA5+ DM-ILD. Methods The series matrix files of DM and NSIP were downloaded from the Gene Expression Omnibus (GEO) database to identify the differentially expressed genes (DEGs). Gene set enrichment analysis (GSEA) was used to screen the common enriched pathways related to DM and NSIP. Next, the co-expressed differential expressed genes (co-DEGs) between MDA5+, MDA5- and NSIP groups were identified by Venn plots, and then selected for different enrichment analyses and protein–protein interaction (PPI) network construction. The mRNA expression levels of IFN-beta and EIF2AK2 were measured by RT-qPCR. The protein expression levels of IFN-beta were measured by ELISA. Results Using GSEA, the enriched pathway “herpes simplex virus 1 infection” was both up-regulated in DM and NSIP. Enrichment analysis in MDA5+ DM, MDA5- DM and NSIP reported that the IFN-beta signalling pathway was an important influencing factor in the MDA5+ DM-ILD. We also identified that eukaryotic translation initiation factor 2 alpha kinase 2 (EIF2AK2) was an important gene signature in the MDA5+ DM-ILD by PPI analysis. The expression levels of IFN-beta and EIF2AK2 were significantly increased in MDA5+ DM-ILD patients. Conclusions IFN-beta and EIF2AK2 contributed to the pathogenesis of MDA5+ DM-ILD, which could be used as potential therapeutic targets.

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The synchronized gene expression of retrotransposons and type I interferon in dermatomyositis

Cited by 4 publications

References 5 publications

Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis

Autophagy-related genes are potential diagnostic biomarkers for dermatomyositis

Coordination of retrotransposons and type I interferon with distinct interferon pathways in dermatomyositis, systemic lupus erythematosus and autoimmune blistering disease

IFN-beta and EIF2AK2 are potential biomarkers for interstitial lung disease in anti-MDA5 positive dermatomyositis

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