Xiao Li-Wei, Yang Min, Dong Jing, Xie Hui, Sui Guo-Liang, He Yu-Ling, Lei Jia-Xuan, Liao Er-Yuan, Yuan Xiao
Stomatological Center, the Second Xiangya Hospital, Central South University, Changsha, China.
Cell Physiol Biochem. 2011;28(2):297-304. doi: 10.1159/000331743. Epub 2011 Aug 16.
To explore the possible role for connective tissue growth factor (CTGF) during tooth movement, we evaluated CTGF gene and protein expression in MG-63 cells subjected to cyclic stretch. Cyclic stretch caused a time-dependent increase in CTGF mRNA and protein levels.Inhibition of p38 MAP kinase or ERK activation did not affect cyclic stretch-induced CTGF expression. Specific inhibitors of PI3K suppressed stretch -induced CTGF expression in a time-dependent manner. cyclic stretch activated JNK and ERK, but not p38 MAP kinase in osteoblast-like cells. PI3K inhibitors suppressed cyclic stretch-induced JNK, but not p38 MAP kinase activation. Finally, SP600125, a Specific Inhibitor of JNK, suppressed stretch -induced CTGF Expression. These results suggest that stretch-induced CTGF expression is mediated through the PI3K-JNK -dependent pathway, not by p38 MAP kinase and ERK pathways.
为了探究结缔组织生长因子（CTGF）在牙齿移动过程中的可能作用，我们评估了受周期性拉伸的MG-63细胞中CTGF基因和蛋白的表达。周期性拉伸导致CTGF mRNA和蛋白水平呈时间依赖性增加。抑制p38丝裂原活化蛋白激酶（MAP激酶）或细胞外信号调节激酶（ERK）的激活并不影响周期性拉伸诱导的CTGF表达。磷脂酰肌醇-3激酶（PI3K）的特异性抑制剂以时间依赖性方式抑制拉伸诱导的CTGF表达。周期性拉伸激活了成骨样细胞中的应激活化蛋白激酶（JNK）和ERK，但未激活p38 MAP激酶。PI3K抑制剂抑制了周期性拉伸诱导的JNK激活，但未抑制p38 MAP激酶的激活。最后，JNK的特异性抑制剂SP600125抑制了拉伸诱导的CTGF表达。这些结果表明，拉伸诱导的CTGF表达是通过PI3K-JNK依赖性途径介导的，而非通过p38 MAP激酶和ERK途径。
