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JYMS : Journal of Yeungnam Medical Science

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HOME > J Yeungnam Med Sci > Volume 24(1); 2007 > Article
Review Identification of Interleukin 1-Responsive Genes in Human Chondrosarcoma SW1354 cells by cDNA Microarray Technology.
Jun Ha Jeon, Yong Wook Jung, Dae Young Yun, Hyun Do Kim, Chang Mo Kwon, Young Hoon Hong, Jae Ryong Kim, Choong Ki Lee
Journal of Yeungnam Medical Science 2007;24(1):24-40
Published online: June 30, 2007
1Department of Internal Medicine, College of Medicine, Yeungnam University, Daegu, Korea.
2Department of Biochemistry and Molecular Biology, College of Medicine, Yeungnam University, Daegu, Korea.
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Accumulating evidence shows that interleukin(IL)-1 plays a critical role in inflammation and connective tissue destruction observed in both osteoarthritis and rheumatoid arthritis. IL-1 induces gene expression related to cytokines, chemokines and matrix metalloproteinases by activation of many different transcription factors. MATERIALS AND METHODS: The chondrosarcoma cell line, SW1353, is known to be a valuable in vitro system for investigating catabolic gene regulation by IL-1beta in chondrocytic cells. To explore and analyze the changes in gene expression by IL-1 responsible for arthritis, SW1353 was treated with IL-1 for 1, 6 and 24 h and then total RNAs were purified for each time. The changes in gene expression were analyzed with 17k human cDNA microarrays and validated by semi-quantitative RT-PCR. RESULTS: Greater than a two-fold change was observed in 1,200 genes including metallothioneins, matrix metalloproteinases, extracellular matrix proteins, antioxidant proteins, cytoskeleton proteins, cell cycle regulatory proteins, proteins for cell growth and apoptosis, signaling proteins and transcription factors. These changes appeared to be correlate with the pathophysiological changes observed in early osteoarthritis. CONCLUSION: cDNA microarray analysis revealed a marked variability in gene expression, and provided insight into the overall molecular changes. The result of this study provide initial information for further studies to identify therapeutic targets in osteoarthritis pathogenesis.

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