NDLI: 243 the Etiology of Kashin-beck Disease (kbd): the Effects of Fungal Mycotoxins on Chondrocyte and Cartilage Metabolism

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243 the Etiology of Kashin-beck Disease (kbd): the Effects of Fungal Mycotoxins on Chondrocyte and Cartilage Metabolism

Content Provider	Semantic Scholar
Author	Cao, Junling Caterson, Bruce Chen, Jean Hong Yue, Yongli Shi, Zhongli Zhang, An zhong Zhang, Zu Peng Fu, Qiang Liu, Feng-Jun Hughes, Colin E.
Copyright Year	2008
Abstract	induced a 10 fold or greater upregulation of several proinflammatory genes, including cytokines Il-1b, Il-6, Il-8, Il-12, Il-17, and mediators, COX-2, iNOS, MMP-1, MMP-3, MMP-4, MMP-7, MMP-9, MMP-13. However, these genes were expressed at negligible to very low density in unstimulated control chondrocytes. Cluster analysis of chondrocytic genes in response to low/physiological DTF showed that these signals markedly regulate genes associated with chondrocyte growth and proliferation, BMP-2, SOX-9, GDF-5, TGF-b, BMP-4, BMP-7, IGF-1, IGF-2; genes associated with cartilage extracellular matrix, proteoglycans and collagens, apoptosis, cell cycle associated genes, signaling cascades, MAP kinases, NF-kB cascade, SMADs, and intracellular structural proteins (actin, tubulin, vimentin, etc), adhesion molecules. Conclusions: The results demonstrate that mechanical signals dynamically cause complex magnitude-dependent gene regulation. Certain gene clusters or representative genes are distinct, whereas others overlap in response to low or high magnitudes of DTF. This differential magnit�pendent gene regulation may play a key role to ultimately allow the remarkable and beneficial/detrimental effects of mechanical signals that are realized at cartilage level. Acknowledgement: NIH AT00646, AR04878, NIDCR DE15399.
File Format	PDF HTM / HTML
DOI	10.1016/S1063-4584(08)60288-5
Volume Number	16
Alternate Webpage(s)	https://core.ac.uk/download/pdf/82260619.pdf
Alternate Webpage(s)	https://doi.org/10.1016/S1063-4584%2808%2960288-5
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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