OBJECTIVE: To elucidate the role of microRNA (miRNA) in the pathogenesis of 
rheumatoid arthritis (RA), we analyzed synoviocytes from RA patients for their 
miRNA expression.
METHODS: Synoviocytes derived from surgical specimens obtained from RA patients 
were compared with those obtained from osteoarthritis (OA) patients for their 
expression of a panel of 156 miRNA with quantitative stem-loop reverse 
transcription-polymerase chain reaction. The miRNA whose expression decreased or 
increased in RA synoviocytes as compared with OA synoviocytes were identified, 
and their target genes were predicted by computer analysis. We used an in vitro 
system of enhancing the expression of specific miRNA by transfection of 
precursors into synoviocytes, and then we performed proliferation, cell cycle, 
and apoptosis assays, as well as enzyme-linked immunosorbent assays for cytokine 
production. The effects of transfection on predicted target protein and 
messenger RNA (mRNA) were then examined by Western blot analysis and luciferase 
reporter assay.
RESULTS: We found that miR-124a levels significantly decreased in RA 
synoviocytes as compared with OA synoviocytes. Transfection of precursor 
miR-124a into RA synoviocytes significantly suppressed their proliferation and 
arrested the cell cycle at the G1 phase. We identified a putative consensus site 
for miR-124a binding in the 3'-untranslated region of cyclin-dependent kinase 2 
(CDK-2) and monocyte chemoattractant protein 1 (MCP-1) mRNA. Induction of 
miR-124a in RA synoviocytes significantly suppressed the production of the CDK-2 
and MCP-1 proteins. Luciferase reporter assay demonstrated that miR-124a 
specifically suppressed the reporter activity driven by the 3'-untranslated 
regions of CDK-2 and MCP-1 mRNA.
CONCLUSION: The results of this study suggest that miR-124a is a key miRNA in 
the posttranscriptional regulatory mechanisms of RA synoviocytes.