[1]路磊 张涛 朱大安 何勇 谢建新 方斌△.胰岛素样生长因子-1保护人终板软骨细胞的作用机制[J].中国中医骨伤科杂志,2020,28(07):11-15.
 LU Lei ZHANG Tao ZHU Daan HE Yong XIE Jianxin FANG Bin.Mechanism of Protective Role of Insulin Growth Factor-1 in Human Endplate Chondrocytes[J].Chinese Journal of Traditional Medical Traumatology & Orthopedics,2020,28(07):11-15.
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胰岛素样生长因子-1保护人终板软骨细胞的作用机制()
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《中国中医骨伤科杂志》[ISSN:1005-0205/CN:42-1340/R]

卷:
第28卷
期数:
2020年07期
页码:
11-15
栏目:
实验研究
出版日期:
2020-07-10

文章信息/Info

Title:
Mechanism of Protective Role of Insulin Growth Factor-1 in Human Endplate Chondrocytes
文章编号:
1005-0205(2020)07-0011-05
作者:
路磊1 张涛1 朱大安1 何勇1 谢建新1 方斌1△
1浙江绍兴市中心医院骨科(浙江 绍兴,312030)
Author(s):
LU Lei1 ZHANG Tao1 ZHU Daan1 HE Yong1 XIE Jianxin1 FANG Bin1△
1 Department of Orthopedics,Shaoxing Central Hospital,Shaoxing 312030,Zhejiang China.
关键词:
椎间盘退变 终板软骨细胞 胰岛素样生长因子-1
Keywords:
intervertebral disc degeneration endplate chondrocytes insulin like growth factor-1
分类号:
R-33
文献标志码:
A
摘要:
目的:明确胰岛素样生长因子-1(IGF-1)保护人终板软骨细胞的作用机制。方法:从腰椎爆裂性骨折患者的终板分离原代终板软骨细胞,用IGF-1刺激原代终板软骨细胞,检测COL2A1,SOX9和MMP13的mRNA水平和蛋白表达水平; 用IGF-1刺激原代终板软骨细胞,检测PI3K活性、AKT和p-AKT蛋白表达,以及ERK1/2和p-ERK1/2的蛋白表达; IGF-1联合PI3K抑制剂LY 294002或ERK1/2抑制剂AG-126处理原代终板软骨细胞,再次检测COL2A1,SOX9和MMP13的蛋白表达,明确其上下游关系。结果:IGF-1可以诱导COL2A1和SOX9上调表达,并抑制MMP13; 此外,IGF-1增高PI3K活性,并上调p-AKT和p-ERK1/2; IGF-1上调COL2A1的作用依赖于PI3K-AKT信号通路的激活,而IGF-1诱导SOX9上调和MMP13下调依赖于ERK1/2的活化。结论:IGF-1激活PI3K-AKT信号通路和ERK1/2通路,调节终板软骨细胞功能性蛋白的表达,为椎间盘退变的治疗提供理论依据。
Abstract:
Objective:To identify the underlying mechanism of protective role of insulin growth factor-1(IGF-1)in endplate chondrocytes. Methods:Primary endplate chondrocytes were isolated from the endplate of patients with lumber burst fracture. The cells were treated with IGF-1 followed by detecting the expression of COL2A1,SOX9 and matrix metallopeptidase 13(MMP13),as well as the activity of phophatidylinositol 3 kinase(PI3K)and the expression of AKT,p-AKT,extracellular signal-regulated kinase 1/2(ERK1/2)and p-ERK1/2. Next,we treated the cells with PI3K inhibitor LY 294002 or ERK1/2 inhibitor AG-126 in the presence of IGF-1 to explore the underlying mechanism. Results:IGF-1 induced upregulation of COL2A1 and SOX9 and downregulation of MMP13 in primary endplate chondrocytes. In addition,IGF-1 could activate PI3K-AKT signaling pathway and ERK1/2. Further investigation revealed that IGF-1-induced upregulation of COL2A1 depended on PI3K-AKT signaling pathway,while IGF-1-induced activation of ERK1/2 was responsible for the upregulation of SOX9 and downregulation of MMP13 in primary endplate chondrocytes. Conclusion:Activation of PI3K-AKT and ERK1/2 by IGF-1 may involve in the expression of functional proteins in endplate chondrocytes,providing a theoretical basis for treatment of intervertebral disc degeneration.

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备注/Memo

备注/Memo:
(收稿日期:2019-10-01)基金项目:绍兴市公益性技术应用研究计划项目(2018C30137) 通信作者 E-mail:llxjmua@163.com
更新日期/Last Update: 2020-07-10