We are analyzing https://link.springer.com/article/10.1186/ar2493.

Title:
Upregulated miR-146a expression in peripheral blood mononuclear cells from rheumatoid arthritis patients | Arthritis Research & Therapy
Description:
Introduction MicroRNAs are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their targeted mRNAs. It is known that aberrant microRNA expression can play important roles in cancer, but the role of microRNAs in autoimmune diseases is only beginning to emerge. In this study, the expression of selected microRNAs is examined in rheumatoid arthritis. Methods Total RNA was isolated from peripheral blood mononuclear cells obtained from patients with rheumatoid arthritis, and healthy and disease control individuals, and the expression of miR-146a, miR-155, miR-132, miR-16, and microRNA let-7a was analyzed using quantitative real-time PCR. Results Rheumatoid arthritis peripheral blood mononuclear cells exhibited between 1.8-fold and 2.6-fold increases in miR-146a, miR-155, miR-132, and miR-16 expression, whereas let-7a expression was not significantly different compared with healthy control individuals. In addition, two targets of miR-146a, namely tumor necrosis factor receptor-associated factor 6 (TRAF6) and IL-1 receptor-associated kinase 1 (IRAK-1), were similarly expressed between rheumatoid arthritis patients and control individuals, despite increased expression of miR-146a in patients with rheumatoid arthritis. Repression of TRAF6 and/or IRAK-1 in THP-1 cells resulted in up to an 86% reduction in tumor necrosis factor-α production, implicating that normal miR-146a function is critical for the regulation of tumor necrosis factor-α production. Conclusions Recent studies have shown that synovial tissue and synovial fibroblasts from patients with rheumatoid arthritis exhibit increased expression of certain microRNAs. Our data thus demonstrate that microRNA expression in rheumatoid arthritis peripheral blood mononuclear cells mimics that of synovial tissue/fibroblasts. The increased microRNA expression in rheumatoid arthritis patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy, but this will require confirmation using a large and well defined cohort. Our data also suggest a possible mechanism contributing to rheumatoid arthritis pathogenesis, whereby miR-146a expression is increased but unable to properly function, leading to prolonged tumor necrosis factor-α production in patients with rheumatoid arthritis.
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expression, patients, mirna, mira, cells, irak, article, arthritis, control, traf, pubmed, levels, pbmcs, rheumatoid, tnfα, disease, increased, google, scholar, figure, individuals, gwb, cas, thp, healthy, patient, synovial, human, data, rna, cell, microrna, factor, shown, usa, qrtpcr, analysis, determined, production, tissue, treatment, blood, compared, mrna, study, necrosis, peripheral, mononuclear, number, tumor,

Topics {✒️}

anti-tnf-α therapy versus quantitative real-time rt-pcr rabbit anti-rck/p54 antibodies goat anti-rabbit igg successful anti-tnf-α therapies ficoll density-gradient centrifugation rna-induced silencing complex quantitative real-time pcr real-time quantitative pcr upregulated mir-146a expression proinflammatory cytokines/chemokines tnf-α tnf-α stimulation induces macrophage colony-stimulating factor nf-b-dependent induction sterile phosphate-buffered saline small interfering rna edward kl chan article download pdf decreased tnf-α production prolonged tnf-α production human anti-gwb serum rheumatoid arthritis patients rheumatoid arthritis pathogenesis 10 ng/ml tnf-α 1 ng/ml tnf-α rnase iii enzymes monocyte/macrophage population adhered post-transcriptional level [4 tumor necrosis factor mirna-mediated regulation [6] rheumatology classification criteria privacy choices/manage cookies osteoarthritis synovial fibroblasts rheumatoid arthritis inflammatory cytokine production mir-146a level authors’ original file mirna analysis exhibited macrophage chemoattractant protein microprocessor complex mediates rna polymerase ii aberrant microrna expression article number r101 increased mirna expression elevated mirna expression rabbit anti-irak-1 rabbit anti-traf6 high expression levels anti-irak-1 antibodies c-reactive protein

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Filipowicz W, Bhattacharyya SN, Sonenberg N: Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight?

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WebPage:
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         headline:Upregulated miR-146a expression in peripheral blood mononuclear cells from rheumatoid arthritis patients
         description:MicroRNAs are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their targeted mRNAs. It is known that aberrant microRNA expression can play important roles in cancer, but the role of microRNAs in autoimmune diseases is only beginning to emerge. In this study, the expression of selected microRNAs is examined in rheumatoid arthritis. Total RNA was isolated from peripheral blood mononuclear cells obtained from patients with rheumatoid arthritis, and healthy and disease control individuals, and the expression of miR-146a, miR-155, miR-132, miR-16, and microRNA let-7a was analyzed using quantitative real-time PCR. Rheumatoid arthritis peripheral blood mononuclear cells exhibited between 1.8-fold and 2.6-fold increases in miR-146a, miR-155, miR-132, and miR-16 expression, whereas let-7a expression was not significantly different compared with healthy control individuals. In addition, two targets of miR-146a, namely tumor necrosis factor receptor-associated factor 6 (TRAF6) and IL-1 receptor-associated kinase 1 (IRAK-1), were similarly expressed between rheumatoid arthritis patients and control individuals, despite increased expression of miR-146a in patients with rheumatoid arthritis. Repression of TRAF6 and/or IRAK-1 in THP-1 cells resulted in up to an 86% reduction in tumor necrosis factor-α production, implicating that normal miR-146a function is critical for the regulation of tumor necrosis factor-α production. Recent studies have shown that synovial tissue and synovial fibroblasts from patients with rheumatoid arthritis exhibit increased expression of certain microRNAs. Our data thus demonstrate that microRNA expression in rheumatoid arthritis peripheral blood mononuclear cells mimics that of synovial tissue/fibroblasts. The increased microRNA expression in rheumatoid arthritis patients is potentially useful as a marker for disease diagnosis, progression, or treatment efficacy, but this will require confirmation using a large and well defined cohort. Our data also suggest a possible mechanism contributing to rheumatoid arthritis pathogenesis, whereby miR-146a expression is increased but unable to properly function, leading to prolonged tumor necrosis factor-α production in patients with rheumatoid arthritis.
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         Orthopedics
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