Christoph Kolling

TL;DR: It is hypothesized that the inflammatory milieu may alter miRNA expression profiles in resident cells of the rheumatoid joints and miR-155 may be involved in modulation of the destructive properties of RASFs.

TL;DR: The findings of high expression of TLRs, particularly TLRs 3 and 4, at an early stage of RA and the reactivity of synovial fibroblasts in vitro to TLR ligands suggest that TLR signaling pathways resulting in persistent inflammation and joint destruction are activated early in the disease process.

TL;DR: Elevated levels of miR-203 lead to increased secretion of MMP-1 and IL-6 via the NF-κB pathway and thereby contribute to the activated phenotype of synovial fibroblasts in RA.

TL;DR: The balance of histone acetylase/HDA activities is strongly shifted toward histone hyperacetylation in patients with RA, and these results offer novel molecular insights into the pathogenesis of the disease that might be relevant to the development of future therapeutic approaches.

TL;DR: Investigation of the expression and effect of the microRNA-34 (miR-34) family on apoptosis in rheumatoid arthritis synovial fibroblasts provided evidence of a methylation-specific down-regulation of proapoptotic miR- 34a* in RASFs.