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

被引:27
|
作者
Song, Yu Wen [1 ]
Zhang, Tao [1 ]
Wang, Wen Bo [1 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 1, Dept Orthoped 3, Harbin, Heilongjiang, Peoples R China
关键词
Glucocorticoid; Chondrocytes; Sox9; Collagen type II (Col II); p38; MAPK; BONE MORPHOGENETIC PROTEIN-2; ARTICULAR CHONDROCYTES; CARTILAGE; EXPRESSION; DIFFERENTIATION; INDUCE; TISSUE; CELLS;
D O I
10.1007/s00296-011-2091-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 mu M. 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.
引用
收藏
页码:3669 / 3673
页数:5
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