Introduction: Rheumatoid arthritis (RA) is a persistent autoimmune disease in which the activity of proinflammatory cytokines and the imbalance, related to the inflammatory process, between elements of bone tissue remodeling such as osteoclasts and osteoblasts play a key role in development of erosions and bone destruction. MicroRNAs are important regulators of skeletal remodeling and are involved in RA pathogenesis. Myomir-206 (miR-206) is unrivalled among the myomirRs, where it is expressed in skeletal muscle and either absent or minimally expressed in other tissues Material and methods: This study was designed to analyze the miR-206 expression pattern in peripheral blood mononuclear cells (PBMCs) using quantitative real time polymerase chain reaction and its correlation with IL-16/IL-17 proinflammatory cytokines in two groups – 20 healthy individuals and 30 patients with RA. Results: Elevated expression of miR-206 was observed in RA patients compared with healthy controls (p < 0.001). A significant increase in both IL-17 and IL-16 serum levels was found in the RA group (p < 0.01 and p < 0.05; respectively) compared to the control group. miR-206 expression level and IL-17 production were directly positively correlated (r = 0.491; p < 0.01). ROC analysis of miR-206 showed a cutoff value of 2.7 with 70% sensitivity, 85% specificity, and the area under the curve was 0.802 (p < 0.001) with the 95% confidence interval from 0. 676 to 0.927 Conclusions: Taken together, our results indicate the importance of miR-206 expression in patients with RA, as a potential new biomarker that affects bone loss/deformity and its collaborative role with proinflammatory cytokines such as IL-16 and IL-17 in RA bone metabolism. Particular interest should be given to further research to determine the contribution of expression of miR-206 in RA pathogenesis
CITATION STYLE
ElAtta, A. A., Ali, Y., Bassyouni, I., & Talaat, R. (2019). Correlation of myomir-206 and proinflammatory cytokines (IL-16 and IL-17) in patients with rheumatoid arthritis. Reumatologia, 57(2), 72–77. https://doi.org/10.5114/reum.2019.84811
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