Autophagy modulates osteoarthritis-related gene expression in human chondrocytes.

摘要: Objective Autophagy, an evolutionarily conserved process for the bulk degradation of cytoplasmic components, serves as a cell survival mechanism. The purpose this study was to elucidate role autophagy in human chondrocytes and pathophysiology osteoarthritis (OA). Methods Autophagy articular cartilage primary assessed using antibodies markers light chain 3 beclin 1. states under catabolic nutritional stresses were examined. We also examined effects inhibition or induction stimulation with interleukin-1β. Autophagy inhibited by small interfering RNA targeting ATG5, induced rapamycin. real-time polymerase reaction aggrecan, COL2A1, MMP13, ADAMTS5 messenger RNA. To further examine mechanism regulation OA chondrocytes, we investigated whether modulates apoptosis reactive oxygen species (ROS). Results Autophagy increased cartilage. Catabolic autophagy. In addition, caused OA-like gene expression changes, while prevented them. Furthermore, amount cleaved poly(ADP-ribose) caspase 9, these increases. ROS activity decreased autophagy. Conclusion These observations suggested that is adaptive response protect cells from stresses, regulates changes through modulation ROS. Further studies about will provide novel insights into OA.