We investigated the effects of advanced glycation end products (AGE) which accumulate in articular cartilage with age in human osteoarthritic chondrocytes. We found AGE-BSA significantly increased MMP-1, -3, and -13, and TNF-α in a dose-dependent manner. AGE-BSA-stimulated JNK, p38, and ERK and NF-κB activity. The stimulatory effect of AGE-BSA on MMP-1, -3, and -13 were reversed by treatment with specific JNK, p38 inhibitors, suggesting JNK and p38 are involved in AGE-BSA-induced MMPs and TNF-α. We also observed that NF-κB is involved in AGE-BSA-induced TNF-α. Pretreatment with soluble receptor for AGE (sRAGE) also reduced AGE-stimulated MMPs and TNF-α, implicating the involvement of receptor for AGE (RAGE). In conclusion, accumulation of AGE may have a role in the development of osteoarthritis by increasing MMP-1, -3, and -13, and TNF-α. © 2007 Federation of European Biochemical Societies.
Nah, S. S., Choi, I. Y., Yoo, B., Kim, Y. G., Moon, H. B., & Lee, C. K. (2007). Advanced glycation end products increases matrix metalloproteinase-1, -3, and -13, and TNF-α in human osteoarthritic chondrocytes. FEBS Letters, 581(9), 1928–1932. https://doi.org/10.1016/j.febslet.2007.03.090