Preptin对成骨细胞结缔组织生长因子表达的影响及其机制研究

目的 探讨Preptin对成骨细胞结缔组织生长因子(CTGF)表达的影响及其机制.方法采用人重组preptin干预人原代成骨细胞,CTGF蛋白水平用Western印迹法检测.丝裂原活化蛋白激酶p38(p38MAPK)、细胞外信号调节激酶(ERK1/2)、c-Jun氨基端激酶(JNK)及其磷酸化水平用Western印迹法检测.在preptin干预前用细胞信号阻断剂(PD98059、SP600125或SB203580)预处理阻断人成骨细胞MAPK信号转导,以分析preptin诱导人成骨细胞CTGF表达的作用机制.结果 Preptin可呈时间和剂量依赖性地促进人成骨细胞CTGF的分泌,并且preptin可诱导人成骨细胞ERK的活化,对p38MAPK或JNK无激活作用;人成骨细胞用ERK抑制剂PD98059预处理可使preptin诱导的CTGF分泌降低.结论Preptin增加CTGF的表达,并通过ERK/MAPK信号途径来介导.

Effect and mechanism of preptin on connective tissue growth factor expression in human osteoblasts

Objective To investigate the effect and mechnism of preptin on connect tissue growth factor (CTGF) in human osteoblasts. Methods Recombinant human preptin was used to treat primary human osteoblasts, and Western blot was used to detect CTGF protein level. Mitogen-activated protein kinase p38(p38MAPK), extracellular signal-regulated kinase (ERK1/2), c-jun N-terminal Kinase (JNK), and their phosphorylation levels were also detected by Western blot. MAPK inhibitors (PD98059, SP600125, or SB203580)were used to elucidate the mechnism of preptin induced expression of CTGF in human osteoblasts. Results Treatment of human osteoblasts with preptin caused a time and dose-dependent increase in CTGF secretion. Preptin induced activation of ERK, but not p38MAPK or JNK in human osteoblasts. Furhermore, pretreatment of human osteoblasts with the ERK inhibitor PD98059 abolished the preptin-induced CTGF secretion. Conclusion Preptin induces CTGF expression in human osteoblasts by means of ERK/MAPK pathway.