Insulin stimulates osteoblast proliferation and differentiation through ERK and PI3K in MG-63 cells

被引:167
作者
Yang, Jianhong [1 ,2 ]
Zhang, Xiolin [2 ]
Wang, Weiwei [2 ]
Liu, Jing [1 ]
机构
[1] Univ Sci & Technol China, Sch Life Sci, Hefei 230026, Peoples R China
[2] Chinese Acad Sci, Grad Univ, Sch Life Sci, Beijing, Peoples R China
关键词
Insulin; osteoblast; differentiation; ERK; PI3K; GROWTH-FACTOR-I; DIABETES-MELLITUS; SIGNALING PATHWAYS; BONE; OSTERIX; OSTEOPENIA; RECEPTORS; KINASE; MECHANISMS;
D O I
10.1002/cbf.1668
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Insulin has been proposed to be an anabolic agent in bone, but the mechanisms underlying insulin effects on osteoblast differentiation are still not clear To explore the mechanisms of action of insulin on osteoblast growth and differentiation. human osteoblastic cell line-MG-63 was used and stimulated by insulin in the presence or absence of ERK inhibitor PD98059. PI3-K inhibitor LY294002, or inhibitor PD98059 LY294002 The results showed that insulin positively regulated the expression of its receptor Insulin stimulated the proliferation of MG-63 cells in a time- and dose-dependent manner and blockade of both MAPK and PI3K pathways could inhibit the cell proliferation In addition. ALP activity, the secretion of type 1 collagen, OC. gene expression, and mineralized nodule formation were increased in the insulin treated group, whereas these indicators were decreased after treatment with blocking agents However, treatment with PI3-K inhibitor LY294002 significantly reversed the down-regulation of Runx2 expression and treatment with ERK inhibitor PD98059 remarkably decreased up-regulation of Osx and IGF-I expression after insulin treatment Therefore. the data obtained from this study suggested that insulin promoted osteoblast proliferation and differentiation through MAPK and PI3K pathway in MG-63 cells Copyright (C) 2010 John Wiley & Sons, Ltd
引用
收藏
页码:334 / 341
页数:8
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