eISSN: 2084-9834
ISSN: 0034-6233
Reumatologia/Rheumatology
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2/2019
vol. 57
 
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Artykuł oryginalny

Correlation of myomir-206 and proinflammatory cytokines (IL-16 and IL-17) in patients with rheumatoid arthritis

Amira Abo ElAtta
,
Yasser Ali
,
Iman Bassyouni
,
Roba Talaat

Data publikacji online: 2019/04/29
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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




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