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Gluococorticoid could influence extracellular matrix synthesis through Sox9 via p38 MAPK pathway

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Abstract

Here, we used glucocorticoid as an apoptosis inducer to study how glucocorticoid could accelerate cartilage degeneration and the responsible signal pathway. Human chondrocytes were isolated from knee joints gave glucocorticoid of different concentrations for 24 h, 48 h, 72 h, or 1 week, and cell viability was determined. Next, Sox9, Collagen type II, Aggrecan protein expression and mRNA transcription were detected by western blot analysis and quantitative real-time PCR, respectively. Glucocorticoid could suppress chondrocyte growth at the concentration of 100 μM. When cultured with glucocorticoid, the expressions of Sox9, Col II, and Aggrecan were depressed time-dependent and dose-dependent, as well as the mRNA transcription. The glucocorticoid-induced p38 inactivation was one mechanism that may response for the inhibition of extracellular matrix synthesis, and these influences appeared earlier than the apoptosis effect.

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Acknowledgments

The authors would like to thank Mr. Shangha Pan, Mr. Bowen Dong, Mr. Guolong Ma and Ms. You Zhou for technically supports.

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The authors declare no conflict of interest.

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Correspondence to Wen Bo Wang.

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Song, Y.W., Zhang, T. & Wang, W.B. Gluococorticoid could influence extracellular matrix synthesis through Sox9 via p38 MAPK pathway. Rheumatol Int 32, 3669–3673 (2012). https://doi.org/10.1007/s00296-011-2091-8

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  • DOI: https://doi.org/10.1007/s00296-011-2091-8

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