期刊
FEBS LETTERS
卷 581, 期 9, 页码 1928-1932出版社
WILEY
DOI: 10.1016/j.febslet.2007.03.090
关键词
advanced glycation end products; matrix metalloproteinase; tumor necrosis factor-alpha; nuclear factor-kappa B; chondrocyte; osteoarthritis
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-alpha in a dose-dependent manner. AGE-BSA-stimulated JNK, p38, and ERK and NF-kappa B 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-alpha. We also observed that NF-kappa B is involved in AGE-BSA-induced TNF-alpha. Pretreatment with soluble receptor for AGE (sRAGE) also reduced AGE-stimulated MMPs and TNF-alpha, 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-alpha. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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