Research Paper Volume 11, Issue 16 pp 6371—6384

MiR-27a promotes the autophagy and apoptosis of IL-1β treated-articular chondrocytes in osteoarthritis through PI3K/AKT/mTOR signaling

Figure 8. Silencing the PI3K expression increased the apoptosis and autophagy of IL-1β-treated chondrocytes, which were impaired by miR-27a inhibition. IL-1β-treated chondrocytes were co-transfected with the miR-27a inhibitor/miR-Scr and shRNA-PI3K/shRNA-NC. (A) PI3K silencing restored the apoptotic levels attenuated by the miR-27a inhibitor. FC analysis and Annexin V-FITC/PI staining were performed to examine the number of early apoptotic IL-1β-treated chondrocytes at 36 h after their transfection. (B) WB was performed to analyze the expression levels of LC3B and p62 in IL-1β-treated chondrocytes. (C) Q-PCR was performed to analyze the mRNA expression of p62 in IL-1β-treated chondrocytes subjected to miR-27a inhibition and/or PI3K silencing. The results are described as the mean ± SD. *P < 0.05, **P < 0.01 vs. indicated group.