ArticleJournal of autoimmunity2017
MicroRNA-155 contributes to enhanced resistance to apoptosis in monocytes from patients with rheumatoid arthritis.
Article in Journal of autoimmunity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 2 of them syntheses that pooled it.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
43 citing papers in PubMed, 2 syntheses or guidelines pooled it, 94 citations in OpenAlex.
- Role of miR-155 in inflammatory autoimmune diseases: a comprehensive review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- Epigenetic Regulation (Including Micro-RNAs, DNA Methylation and Histone Modifications) of Rheumatoid Arthritis: A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Monocyte/Macrophage Abnormalities Specific to Rheumatoid Arthritis Are Linked to miR-155 and Are Differentially Modulated by Different TNF Inhibitors.Journal of immunology (Baltimore, Md. : 1950) · 2019Trial
- miR-155-SOCS1-Telomere Length Axis: A Tripartite and Multifaceted Approach To Understanding Rheumatoid Arthritis Pathophysiology.Cell biochemistry and biophysics · 2026Article
- Loss of synovial tissue macrophage homeostasis precedes rheumatoid arthritis clinical onset.Science advances · 2024Article
- Expression of miR-155 in monocytes of people with migraine: association with phenotype, disease severity and inflammatory profile.The journal of headache and pain · 2024Article
- Revealing the impact of autophagy-related genes in rheumatoid arthritis: Insights from bioinformatics.Heliyon · 2024Article
- Epigenetic changes in inflammatory arthritis monocytes contribute to disease and can be targeted by JAK inhibition.Rheumatology (Oxford, England) · 2023Article
- Comprehensive overview of microRNA function in rheumatoid arthritis.Bone research · 2023Review
- Bidirectional cytokine-microRNA control: A novel immunoregulatory framework in leishmaniasis.PLoS pathogens · 2022Review
- Preparation of a miR-155-activating nucleic acid nanoflower to study the molecular mechanism of miR-155 in inflammation.Molecular medicine (Cambridge, Mass.) · 2022Article
- miR-155-overexpressing monocytes resemble HLAhighISG15+ synovial tissue macrophages from patients with rheumatoid arthritis and induce polyfunctional CD4+ T-cell activation.Clinical and experimental immunology · 2022Article
- The Effect of α7nAChR Signaling on T Cells and Macrophages and Their Clinical Implication in the Treatment of Rheumatic Diseases.Neurochemical research · 2022Review
- Review
- New Druggable Targets for Rheumatoid Arthritis Based on Insights From Synovial Biology.Frontiers in immunology · 2022Review
- Transient Focal Cerebral Ischemia Leads to miRNA Alterations in Different Brain Regions, Blood Serum, Liver, and Spleen.International journal of molecular sciences · 2021Article
- MiR-499a prevents astrocytes mediated inflammation in ischemic stroke by targeting PTEN.Non-coding RNA research · 2021Article
- Nutrition and Rheumatoid Arthritis in the 'Omics' Era.Nutrients · 2021Review
- Association study between immune-related miRNAs and mixed connective tissue disease.Arthritis research & therapy · 2021Article
- Exploring the Extracellular Vesicle MicroRNA Expression Repertoire in Patients with Rheumatoid Arthritis and Ankylosing Spondylitis Treated with TNF Inhibitors.Disease markers · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Monocytes and macrophages are key mediators of inflammation in rheumatoid arthritis (RA). Their persistence at the inflammatory site is likely to contribute to immunopathology. We sought to characterise one mechanism by which persistence may be achieved: resistance to apoptosis and the role of mir-155 in this process. CD14+ monocytes from peripheral blood (PBM) and synovial fluid (SFM) of RA patients were found to be resistant to spontaneous apoptosis relative to PBM from healthy control (HC) individuals. RA SFM were also resistant to anti-Fas-mediated apoptosis and displayed a gene expression profile distinct from HC and RA PBM populations. Gene expression profiling analysis revealed that the differentially expressed genes in RA SFM vs. PBM were enriched for apoptosis-related genes and showed increased expression of the mir-155 precursor BIC. Following identification of potential mir-155 target transcripts by bioinformatic methods, we show increased levels of mature mir-155 expression in RA PBM and SFM vs. HC PBM and a corresponding decrease in SFM of two predicted mir-155-target mRNAs, apoptosis mediators CASP10 and APAF1. Using miR mimics, we demonstrate that mir-155 over-expression in healthy CD14+ cells conferred resistance to spontaneous apoptosis, but not Fas-induced death in these cells, and resulted in increased production of cytokines and chemokines. Collectively our data indicate that CD14+ cells from patients with RA show enhanced resistance to apoptosis, and suggest that an increase in mir-155 may partially contribute to this phenotype.
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Registered trials
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