摘要
目的探讨周期性机械应力促进大鼠软骨细胞增殖和细胞外基质合成的细胞外调节蛋白激酶(ERK)1/2信号传导机制。方法取第二代大鼠软骨细胞,随机分为预处理组和对照组。预处理组采用上皮生长因子受体(EGFR)特异性抑制剂(AG1478)阻断EGFR的活化;对照组不给予特殊预处理。两组细胞分别在有、无周期性机械应力条件下培养,1h后采用Western blot检测ERK1/2的表达和磷酸化水平;8h后采用Real-time PCR检测aggrecan和Ⅱ型胶原的基因表达水平。两组细胞分别在有、无周期性机械应力条件下每天培养8h,连续3d后采用CCK-8法检测细胞增殖。结果当EGFR被抑制以后,周期性机械应力促进的软骨细胞增殖和细胞外基质合成均显著降低,而且ERK1/2的磷酸化水平也下降(P<0.05)。结论周期性机械应力通过激活EGFRERK1/2信号通路促进大鼠软骨细胞增殖和细胞外基质合成。
Objective To explore the mechanism for periodic mechanical stress to promote ERK1/2 signal transduction in rat chondrocyte proliferation and matrix synthesis. Methods Rat chondrocytes derived from the second generation were treated with AG1478 （pretreatment group）and an equivalent amount of DMSO （0.1%, v/v, as control group）. The cells were maintained under periodic mechanical stress or static conditions for 1 h prior to Western blot analysis and for 8 h prior to Real-time PCR analysis, respectively. The cells were cultured for 3 days under periodic mechanical stress or static conditions 8 h per day prior to CCK-8 assay, respectively. Results The pretreatment of EGFR selective inhibitor AG1478 reduced periodic mechanical stress-induced choadrocyte proliferation and matrix synthesis （P〈0. 05）, and attenuated the phosphorylation of ERK1/2-Thr202/Tyr^204 （P〈0. 05）. Conclusion Periodic mechanical stress promotes chondrocyte proliferation and matrix synthesis via activating EGFR-ERK1/2 signal pathway in rat chondrocytes.
出处
《江苏医药》
CAS
北大核心
2013年第21期2526-2528,共3页
Jiangsu Medical Journal
关键词
周期性机械应力
软骨细胞
Periodic mechanical stress
Chondrocytes
