miR-146a attenuates the transforming growth factor-β signaling pathway. (A) C5.18 cells were co-transfected with miR-146a and p3TP-lux reporter plasmid followed by treatment with or without exogenous transforming growth factor (TGF)-β1 (10 ng/ml) for 4 hours. The cell lysates were obtained to determine the luciferase activity. Values are the mean ± standard deviation of at least three independent experiments. **P < 0.01. NC, negative control. (B) Overexpression of miR-146a blocked TGF-β1-stimulated activation of extracellular signal-regulated kinase (ERK). Chondrocytes were transfected with miR-146a mimics, and, after serum starvation, cells were treated with TGF-β1 (10 ng/ml) for the indicated periods. Cell lysates were analyzed for phosphorylated and total ERK levels in chondrocytes.
Li et al. Arthritis Research & Therapy 2012 14:R75 doi:10.1186/ar3798