ArticleEpigenetics2020
Identification of PBMC-expressed miRNAs for rheumatoid arthritis.
Article in Epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Multidimensional regulatory mechanisms and translational potential of epigenetic networks in the rheumatoid arthritis disease course.Frontiers in immunology · 2026Review
- The Dual Role ofBiology · 2025Review
- Identification of miR-190a-5p and miR-26b-5p as Potential microRNA Biomarkers for Psoriatic Arthritis.ACR open rheumatology · 2025Article
- Expression profiles of miR-101-3p and miR-431-5p as potential diagnostic biomarkers for rheumatoid arthritis.Scientific reports · 2025Article
- Functional Significance of miR-4693-5p in Targeting HIF1α and Its Link to Rheumatoid Arthritis Pathogenesis.Non-coding RNA · 2024Article
- Cell Cultures as a Versatile Tool in the Research and Treatment of Autoimmune Connective Tissue Diseases.Cells · 2023Review
- PDCD5 as a Potential Biomarker for Improved Prediction of the Incidence and Remission for Patients with Rheumatoid Arthritis.Rheumatology and therapy · 2023Article
- Biomarkers (mRNAs and non-coding RNAs) for the diagnosis and prognosis of rheumatoid arthritis.Frontiers in immunology · 2023Review
- Molecular Beacon for Detection miRNA-21 as a Biomarker of Lung Cancer.International journal of molecular sciences · 2022Article
- Identification of novel rheumatoid arthritis-associated MiRNA-204-5p from plasma exosomes.Experimental & molecular medicine · 2022Article
- An update on epigenetic regulation in autoimmune diseases.Journal of translational autoimmunity · 2022Article
- MicroRNA-Mediated Epigenetic Regulation of Rheumatoid Arthritis Susceptibility and Pathogenesis.Frontiers in immunology · 2022Review
- ST3GAL3 Promotes the Inflammatory Response of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis by Activating the TLR9/MyD88 Pathway.Mediators of inflammation · 2022Article
- Dysregulated microRNA expression in rheumatoid arthritis families-a comparison between rheumatoid arthritis patients, their first-degree relatives, and healthy controls.Clinical rheumatology · 2021Article
- Role of microRNA Shuttled in Small Extracellular Vesicles Derived From Mesenchymal Stem/Stromal Cells for Osteoarticular Disease Treatment.Frontiers in immunology · 2021Review
- MicroRNA Variants and HLA-miRNA Interactions are Novel Rheumatoid Arthritis Susceptibility Factors.Frontiers in genetics · 2021Article
- Transcription factor NF-κB promotes acute lung injuryThe Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-transcriptional regulation by miRNAs plays an important role in the pathogenesis of rheumatoid arthritis (RA), however, the roles of specific miRNAs in RA pathogenesis remain largely unclear. This study performed dual-omics (miRNA and mRNA) integration analysis and in-depth cellular and molecular functional exploration to identify novel RA-associated miRNAs and to understand their underlying pathogenic mechanism. Based on the miRNA and mRNA expression profiles in peripheral blood mononuclear cells (PBMCs) from a discovery sample set (25 RA cases and 18 healthy controls), 18 differentially expressed miRNAs (DEMIRs) (|Fold-change|>2 and P < 0.05) were identified and corresponding interaction networks of DEMIRs and mRNA were constructed. After the expression validation of the DEMIRs in a validation sample set (35 RA cases and 35 healthy controls), miR-99b-5p was highlighted. The over-expression of newly discovered miR-99b-5p is able to suppress T cell apoptosis, promote cell proliferation and activation, increase expression of proinflammatory cytokines (IL-2, IL-6, TNF-α, and IFN-γ), and inhibit expression of its target genes mTOR and RASSF4. This study comprehensively identified PBMC-expressed miRNAs along with corresponding regulatory networks significant for RA and discovered miR-99b-5p as a novel post-transcriptional mediator involved in RA pathogenesis. The findings improved our understanding of RA pathogenesis and provided novel insights into the molecular mechanisms underlying RA pathogenesis.
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