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Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants
Published on: January 7, 2019
Advanced oxidation protein products induce apoptosis of human chondrocyte through reactive oxygen species-mediated
Wenbin Ye1, Siyuan Zhu1, Congrui Liao1
1Department of Orthopaedic Spinal Surgery, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Avenue, Guangzhou, 510515, China.
Abstract:
Advanced oxidation production products (AOPPs) have been confirmed to accumulate in patients with rheumatoid arthritis (RA). Previous study demonstrated that AOPPs could accelerate cartilage destruction in rabbit arthritis model. However, the effect of AOPP stimulation on apoptosis of human chondrocyte and the underlying mechanisms remains unclear. This study demonstrated that exposure of chondrocyte to AOPPs resulted in cell apoptosis. AOPP stimulation triggered reactive oxygen species (ROS) production, which induced mitochondrial dysfunction and endoplasmic reticulum stress (ER stress) resulted in caspase activation. Furthermore, an antioxidant, N-acetylcysteine, markedly blocked these signals. Our study demonstrated that AOPPs induce apoptosis via ROS-related mitochondria- and ER-dependent signals in human chondrocyte. Targeting AOPP-triggered ROS generation might be as a promising option for patients with RA.
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