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首页> 外文期刊>Cellular Physiology and Biochemistry >Stretch-inducible Expression of Connective Tissue Growth Factor (CTGF) in Human Osteoblasts-like Cells is Mediated by PI3K-JNK Pathway
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Stretch-inducible Expression of Connective Tissue Growth Factor (CTGF) in Human Osteoblasts-like Cells is Mediated by PI3K-JNK Pathway

机译:PI3K-JNK通路介导人成骨细胞样细胞中结缔组织生长因子(CTGF)的拉伸诱导表达。

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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.
机译:为了探讨结缔组织生长因子(CTGF)在牙齿移动过程中的可能作用,我们评估了CTGF基因和蛋白质在MG-63细胞经受周期性拉伸后的表达。循环拉伸导致CTGF mRNA和蛋白水平随时间增加。抑制p38 MAP激酶或ERK激活并不影响循环拉伸诱导的CTGF表达。 PI3K的特定抑制剂以时间依赖性方式抑制牵张诱导的CTGF表达。环状拉伸激活成骨细胞样细胞中的JNK和ERK,但不激活p38 MAP激酶。 PI3K抑制剂抑制循环拉伸诱导的JNK,但不抑制p38 MAP激酶激活。最终,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,而不是通过p38 MAP激酶和ERK途径介导的。

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