中国组织工程研究

中国组织工程研究

• 骨组织构建 bone tissue construction • 上一篇    下一篇

牵张应力介导细胞成骨分化及相关基因的表达

刘名燕1，李  燕1，钱  红2，冯云霞1，段银钟2，李永明2   

  1. 1山西医科大学口腔系，山西省太原市  030001；2解放军第四军医大学口腔医学院正畸科，陕西省西安市  710032
  • 修回日期:2013-10-23 出版日期:2013-12-10 发布日期:2013-12-10
  • 通讯作者: 李永明，博士，副教授，研究生导师，解放军第四军医大学口腔医学院正畸科，陕西省西安市 710032 liyongming@fmmu.edu.cn
  • 作者简介:刘名燕☆，女，1975年生，山西省长治市人，汉族，2012年解放军第四军医大学毕业，博士，主要从事口腔正畸生物力学研究。 mlinda123@163.com
  • 基金资助:

    国家自然科学基金资助项目(30970697，31370943)*；山西医科大学博士启动基金项目(B03201219)*

Osteogenic differentiation and related gene expression mediated by mechanical strain

Liu Ming-yan1, Li Yan1, Qian Hong2, Feng Yun-xia1, Duan Yin-zhong2, Li Yong-ming2   

  1. 1Dental Department, Shanxi Medical University, Taiyuan  030001, Shanxi Province, China; 2Department of Orthodontics, College of Stomatology, the Fourth Military Medical University, Xi’an  710032, Shaanxi Province, China
  • Revised:2013-10-23 Online:2013-12-10 Published:2013-12-10
  • Contact: Li Yong-ming, M.D., Associate professor, Master’s supervisor, Department of Orthodontics, College of Stomatology, The Fourth Military Medical University, Xi’an 710032, Shaanxi Province, China liyongming@fmmu.edu.cn
  • About author:Liu Ming-yan☆, M.D., Dental Department, Shanxi Medical University, Taiyuan 030001, Shanxi Province, China mlinda123@163.com
  • Supported by:

    the National Natural Science Foundation of China, No. 30970697*, 31370943*; the Doctoral Priming Foundation of Shanxi Medical University in China, No. B03201219*

PDF

427

被引次数

4

摘要：

背景：ERK1/2信号通路和核因子κB信号通路是否参与了牵张应力作用下MC3T3-E1细胞成骨分化及相关基因表达的调控，尚不清楚。
目的：观察机械牵张应力对作用下ERK1/2和核因子κB通路对成骨细胞碱性磷酸酶、Ⅰ型胶原、骨钙蛋白、白细胞介素6表达的影响，探讨ERK1/2与核因子κB信号通路对成骨细胞分化的调控作用。
方法：体外培养的MC3T3-E1细胞，以ERK1/2通路特异性抑制剂PD098059及核因子κB通路抑制剂PDTC分别处理30 min后加载12%的拉伸应变率24 h，以正常细胞及单纯加载12%牵张应力24 h为对照。采用ELISA及Real-time PCR方法检测细胞加载前后碱性磷酸酶活性、Ⅰ型胶原、骨钙蛋白及白细胞介素6 mRNA的表达。
结果与结论：在12%牵张应力作用下，MC3T3-E1细胞碱性磷酸酶、Ⅰ型胶原、白细胞介素6的表达受ERK1/2信号通路的调控，而骨钙蛋白基因表达的变化不受ERK1/2通路的影响。核因子κB信号通路抑制剂PDTC可显著抑制机械牵应张力作用下MC3T3-E1细胞碱性磷酸酶活性的降低，同时抑制白细胞介素6基因的表达，而Ⅰ型胶原、骨钙蛋白基因表达的变化不受核因子κB信号通路的影响。结果表明牵张应力可以通过ERK1/2和核因子κB通路影响MC3T3-E1细胞的成骨分化及相关基因表达。



中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程


全文链接：

关键词: 组织构建, 骨组织构建, 牵张应力, 成骨细胞, ERK1/2, 核因子κB, 信号转导, 碱性磷酸酶, Ⅰ型胶原, 白细胞介素6, 国家自然科学基金

Abstract:

BACKGROUND: The regulatory role of extracellular signal regulated kinase 1/2 (ERK1/2) and nuclear factor kappa B (NF-κB) signal pathways in the osteogenic differentiation of MC3T3-E1 cells subjected to mechanical strain remains unclear.
OBJECTIVE: To investigate the effects of ERK1/2 and NF-kB signal pathway on alkaline phosphatase, type Ⅰ collagen, osteocalcin and interleukin-6 expression in osteoblasts in response to mechanical strain, and to explore the regulatory effects of ERK1/2 and NF-kB signal pathway on osteoblast differentiation.
METHODS: MC3T3-E1 cells cultured in vitro were separately treated with ERK1/2 pathway specific inhibitor PD098059 and NF-kB pathway inhibitor PDTC for 30 minutes, and subjected to12% elongation for 24 hours. Normal cells and cells along loading 12% mechanical strain for 24 hours were considered as controls. Enzyme linked immunosorbent assay and real-time PCR were utilized to detect alkaline phosphatase activities, type Ⅰ collagen, osteocalcin and interleukin-6 mRNA expression before and after cell loading.
RESULTS AND CONCLUSION: Under 12% mechanical strain, alkaline phosphatase, type I collagen, and interleukin-6 expression was regulated by ERK1/2 signal pathway in MC3T3-E1 cells, but osteocalcin gene expression was not affected by ERK1/2 pathway. NF-kB signal pathway inhibitor PDTC significantly suppressed alkaline phosphatase activities in MC3T3-E1 cells under mechanical strain, and inhibited interleukin-6 gene expression. However, type I collagen and osteocalcin gene expression was not affected by NF-kB signal pathway. Results suggested that mechanical strain affected osteogenic differentiation and relevant gene expression in MC3T3-E1 cells by ERK1/2 and NF-kB signal pathway.



中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程


全文链接：

Key words: stress, mechanical, osteoblasts, NF-kB, alkaline phosphatase, type Ⅰ collagen, interleukin-6

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