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MAPK-ERK1/2信号通路调控成骨性基因表达和细胞增殖

丁道芳 李玲慧 宋奕 杜国庆 卫晓恩 曹月龙

南方医科大学学报Issue(10):1432-1436,5.
南方医科大学学报Issue(10):1432-1436,5.

MAPK-ERK1/2信号通路调控成骨性基因表达和细胞增殖

MAPK-ERK1/2 signaling pathway regulates osteogenic gene expression in rat osteoblasts in vitro

丁道芳 1李玲慧 2宋奕 1杜国庆 2卫晓恩 1曹月龙2

作者信息

  • 1. 上海中医药大学附属曙光医院石氏伤科医学中心,上海 201203
  • 2. 上海市中医药研究院骨伤科研究所,上海 201203
  • 折叠

摘要

Abstract

Objective To investigate the effect of inhibition and activation of MAPK-ERK1/2 pathway on the expression of osteogenic genes and proliferation of rat osteoblasts in vitro. Methods Primarily cultured rat osteoblasts, identified by cell morphology studies and ALP staining, were exposed to 1%or 5%rat serum for 24 h or to the specific MAPK-ERK1/2 inhibitor PD0325901. The downstream molecules of MAPK-ERK1/2 pathway including p-ERK1/2 and ERK1/2, osteogenic genes such as Runx2 and Type I collagen, and proliferating cell nuclear antigen (PCNA) were detected by Western Blotting, and alkaline phosphatase activities were analyzed quantitatively. Results Compared with 1%rat serum-treated cells, exposure of the cells to a higher concentration (5%) of rat serum caused a significantly increased phosphorylation level of p-ERK1/2 (P<0.05) and obviously enhanced expressions of the osteogenic genes (Runx2, type I collagen and ALP) and PCNA (P<0.05). Inhibition of the MAPK-ERK1/2 pathway with PD0325901 resulted in suppressed expressions of the osteogenic genes and PCNA. Conclusion The activation of MAPK-ERK1/2 pathway promotes the expression of osteogenic genes such as Runx2, type I collagen and ALP and enhances the proliferative activity of the osteoblasts, while inhibition of this pathway suppresses the expressions of these genes and the cell proliferation, suggesting that this pathway may potentially serve as a therapeutic target for osteoporosis.

关键词

原代成骨细胞/成骨性基因表达/大鼠血清/信号通路

Key words

primary osteoblasts/osteogenic expression/rat serum/signal pathway

引用本文复制引用

丁道芳,李玲慧,宋奕,杜国庆,卫晓恩,曹月龙..MAPK-ERK1/2信号通路调控成骨性基因表达和细胞增殖[J].南方医科大学学报,2013,(10):1432-1436,5.

基金项目

国家自然科学基金(81073114,81072830);上海市教育委员会创新项目(11YZ64);上海市高校青年教师培养资助计划(ZZszy12017) Supported by National Natural Science Foundation of China (81073114,81072830) (81073114,81072830)

南方医科大学学报

OA北大核心CSCDCSTPCDMEDLINE

1673-4254

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