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- W4200538749 abstract "Osteoarthritis (OA) is a common degenerative joint disease. The pathological changes of chondrocytes involve oxidative stress, the pro-inflammatory response, and pro-apoptotic events. Galectin-3 (Gal-3) is a 35 kDa protein with a special chimeric structure. Gal-3 participates in the progression of many diseases, such as cancer metastasis and heart failure. A previous study demonstrated that Gal-3 expression in human cartilage with OA is increased. However, the role of Gal-3 in chondrocyte dysfunction in joints is still unclear. In this study, we applied Gal-3 (5-20 μg/ml) to TC28a2 human chondrocyte cells for 24 h to induce chondrocyte dysfunction. We found that Gal-3 upregulated TLR-4 and MyD88 expression and NADPH oxidase, thereby increasing intracellular ROS in the chondrocytes. Gal-3 increased phosphorylated MEK1/2 and ERK levels, and promoted NF-κB activity. This activation of NF-κB was reduced by silencing TLR-4 and NOX-2. In addition, Gal-3 caused apoptosis of chondrocytes through the mitochondrial-dependent pathway via the TLR-4/NADPH oxidase/MAPK axis. Our study proves the pathogenic role of Gal-3 in Gal-3-induced chondrocyte dysfunction and injuries." @default.
- W4200538749 created "2021-12-31" @default.
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- W4200538749 date "2021-12-11" @default.
- W4200538749 modified "2023-09-24" @default.
- W4200538749 title "Galectin‐3 facilitates inflammation and apoptosis in chondrocytes through upregulation of the <scp>TLR</scp> ‐4‐mediated oxidative stress pathway in <scp>TC28a2</scp> human chondrocyte cells" @default.
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- W4200538749 doi "https://doi.org/10.1002/tox.23414" @default.
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