Role of miR-146a in human chondrocyte apoptosis in response to mechanical pressure injury in vitro

摘要: MicroRNA (miR)-146a is known to be overexpressed in osteoarthritis (OA). However, the role of miR-146a OA has not yet been fully elucidated. In present study, we applied mechanical pressure 10 MPa human chondrocytes for 60 min order investigate expression and apoptosis following injury. Normal were transfected with an mimic or inhibitor regulate expression. Potential target genes predicted using bioinformatics. Moreover, luciferase reporter assay confirmed that Smad4 was a direct miR-146a. The levels miR-146a, vascular endothelial growth factor (VEGF) quantified by quantitative reverse transcription PCR and/or western blot analysis. effects on detected Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry. results indicated affected chondrocyte viability induced early chondrocytes. Mechanical injury increased VEGF decreased chondrocytes, upregulation apoptosis, upregulated downregulated addition, knockdown reduced cell identified as harboring miR‑146a binding sequence 3'-untranslated region (3'-UTR) its mRNA. Furthermore, mediated subjected These demonstrated our model experimentally injury, accompanied downregulation vitro. data suggest involved response may contribute well pathogenesis increasing damaging transforming (TGF)-β signaling pathway through targeted inhibition cartilage.