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-alpha production, implicating that normal miR-146a function is 
critical for the regulation of tumor necrosis factor-alpha 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-alpha 
production in patients with rheumatoid arthritis.