Research Paper Volume 16, Issue 3 pp 2702—2714

Figure 4. Schematic overview of the working model for regulation of miR-146a in tendinopathy. In human and rat tendinopathic tendons, miR-146a expression was examined by qRT-PCR and in situ hybridization. Compared with healthy controls, miR-146a expression was significantly lower. In tendinopathic tendons, miR-146a-positive cell ratio was negatively correlated with the severity of tendinopathy. Over-expression of miR-146a through lentivirus-mediated gene transduction (LVmiR-146a) ameliorates senescence and SASPs in IL-1β stimulated tendinopathic tenocytes by reducing the levels of p53, p16, p21, IL-6, MMP-1, and-3. The anti-inflammatory effect is achieved by lowering the levels of phospho-NF-ĸB and COX-2. Furthermore, in the present experimental settings, overexpression of miR-146a downregulates the expression levels of target molecules, including IRAK-4 and TRAF6.