ArticlePloS one2017
The Impact of MicroRNA-223-3p on IL-17 Receptor D Expression in Synovial Cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- microRNAs as Biomarkers and Therapeutic Targets in Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- New bitongling regulates gut microbiota to predict angiogenesis in rheumatoid arthritis via the gut-joint axis: a deep neural network approach.Frontiers in microbiology · 2025Article
- MicroRNAs as Key Regulators in RA and SLE: Insights into Biological Functions.Current pharmaceutical design · 2024Review
- Review
- Prediction and analysis of microRNAs involved in COVID-19 inflammatory processes associated with the NF-kB and JAK/STAT signaling pathways.International immunopharmacology · 2021Review
- Interleukin-17 receptor D (Sef) is a multi-functional regulator of cell signaling.Cell communication and signaling : CCS · 2021Review
- miR-223: An Effective Regulator of Immune Cell Differentiation and Inflammation.International journal of biological sciences · 2021Review
- Regulation of Osteoclastogenesis and Bone Resorption by miRNAs.Frontiers in cell and developmental biology · 2021Review
- Reduced Platelet miR-223 Induction in Kawasaki Disease Leads to Severe Coronary Artery Pathology Through a miR-223/PDGFRβ Vascular Smooth Muscle Cell Axis.Circulation research · 2020Article
- Aerobic Exercise Inhibits CUMS-Depressed Mice Hippocampal Inflammatory Response via Activating Hippocampal miR-223/TLR4/MyD88-NF-κB Pathway.International journal of environmental research and public health · 2020Article
- Expression of microRNAs in the plasma of patients with acute gouty arthritis and the effects of colchicine and etoricoxib on the differential expression of microRNAs.Archives of medical science : AMS · 2019Article
- Functional Regulation of Macrophage Phenotypes by MicroRNAs in Inflammatory Arthritis.Frontiers in immunology · 2019Review
- Article
- Common microRNA⁻mRNA Interactions in Different Newcastle Disease Virus-Infected Chicken Embryonic Visceral Tissues.International journal of molecular sciences · 2018Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveRheumatoid arthritis (RA) is an autoimmune inflammatory disease affecting joints. Elevated plasma levels of microRNA-223-3p (miR-223-3p) in patients with RA are implicated in the pathogenesis of the disease. This study aimed to analyze the functional role of miR-223-3p in the pathogenesis of RA by overexpressing miR-223-3p in synovial cell lines.
methodsArthritis was induced in the RA model of SKG mice by injection of ß-glucan. The histopathologic features of joints were examined using hematoxylin and eosin and immunohistochemical staining. Plasma levels of miRNA were determined by panel real-time PCR analysis. Target genes of the differentially expressed miRNAs in SKG mice were analyzed using miRNA target prediction algorithms. The dual-luciferase reporter system was used to evaluate the relationship between miR-223-3p and IL-17 receptor D (IL-17RD). The activity of miR-223-3p was analyzed by transfection of plasmid vectors overexpressing miR-223-3p into IL-17RD-expressing NIH3T3 and MH7A cell lines. Il6 and Il17rd mRNA expression was analyzed by quantitative real-time PCR. IL-17RD protein expression was analyzed by western blot analysis.
resultsWe identified 17 upregulated miRNAs (fold change > 2.0) in plasma of SKG mice injected with ß-glucan relative to untreated SKG mice. Il17rd was identified as the candidate target gene of miR-223-3p using five miRNA target prediction algorithms. The transfection of plasmid vectors overexpressing miR-223-3p into NIH3T3 and MH7A cells resulted in the downregulation of Il17rd expression and upregulation of Il6 expression. Expression of miR-223-3p and Il6 mRNA in MH7A cells was upregulated; however, that of Il17rd mRNA was downregulated following TNF-α stimulation. IL-17RD expression in synovial tissues from SKG mice and RA patients was inversely correlated with the severity of arthritis.
conclusionThis study is the first to demonstrate that miR-223-3p downregulates IL-17RD in both mouse and human cells; miR-223-3p may contribute to the pathogenesis of RA by downregulating the expression of IL-17RD and upregulating that of IL-6 in synovial cells.
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