New concepts of therapy highlight an early use of effective treatment to prevent further joint damage in RA. Altered expression of epigenetic marks like miRs offers us the possibility to develop new diagnostic tools and novel therapeutic targets.
We found miR-146, -155 and -203 to be upregulated in rheumatoid arthritis (RA) synovial fibroblasts (SF) compared to osteoarthritis (OA) SF [1,2]. Based on the comprehensive analysis of the expression of 260 miRs we found miR-196a to be one of the most downregulated miRs in RASF. In peripheral blood mononuclear cells, miR-132 and -223 are upregulated in established RA compared with healthy controls (HC) [3,4].
Our aim was to analyze miRs as potential systemic markers in early stages of the disease and to find new miRs locally at the site of inflammation that play a role in the pathogenesis of RA.