Mithramycin downregulates proinflammatory cytokine-induced matrix metalloproteinase gene expression in articular chondrocytes
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05/01/2007
05/01/2007
2005
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Resumo |
Affiliation: Département de Médecine, Faculté de médecine, Université de Montréal & Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CHUM), Hôpital Notre-Dame du CHUM Interleukin-1 (IL-1), IL-17 and tumor necrosis factor alpha (TNF-a) are the main proinflammatory cytokines implicated in cartilage breakdown by matrix metalloproteinase (MMPs) in arthritic joints. We studied the impact of an anti-neoplastic antibiotic, mithramycin, on the induction of MMPs in chondrocytes. MMP-3 and MMP-13 gene expression induced by IL-1ß, TNF-a and IL-17 was downregulated by mithramycin in human chondrosarcoma SW1353 cells and in primary human and bovine femoral head chondrocytes. Constitutive and IL-1-stimulated MMP-13 levels in bovine and human cartilage explants were also suppressed. Mithramycin did not significantly affect the phosphorylation of the mitogen-activated protein kinases, extracellular signal-regulated kinase, p38 and c-Jun N-terminal kinase. Despite effective inhibition of MMP expression by mithramycin and its potential to reduce cartilage degeneration, the agent might work through multiple unidentified mechanisms. |
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1169657 bytes application/pdf |
Identificador |
Liacini, A., Sylvester, J., Li, W., & Zafarullah, M. (2005). Mithramycin downregulates proinflammatory cytokine-induced matrix metalloproteinase gene expression in articular chondrocytes. Arthritis Research & Therapy, 7(4), R777 - R783. 1478-6354 http://dx.doi.org/10.1186/ar1735 |
Direitos |
Ceci est un article en accès libre diffusé sous une licence Creative Commons Paternité laquelle permet une libre utilisation, diffusion et reproduction de l'article sous toutes formes, à la condition de l'attribuer à l'auteur en citant son nom. This is an open access article distributed under the terms of the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/2.0 |
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Article |