[Smad信号通路在转化生长因子-β1介导的成牙本质细胞系MDPC-23中Smad7基因转录中的作用]
[Role of Smad signaling in transcription of Smad7 gene mediated by TGF-beta1 in odontoblast cell line MDPC-23].
作者信息
He Wen-xi, Niu Zhong-ying, Zhao Shou-liang, Zang Xiao-xia, Gao Jie, Li Ping
机构信息
Department of Conservative Dentistry, College of Stomatology, The Fourth Military Medical University, Xi'an 710032, China.
出版信息
Shanghai Kou Qiang Yi Xue. 2005 Apr;14(2):143-6.
PURPOSE
To investigate the role of Smad signaling in transcription of Smad7 gene mediated by TGF-beta1 in odontoblast cell line MDPC-23, and to explore the molecular mechanism of Smad7 gene expression mediated by TGF-beta1 at the transcriptional level.
METHODS
Smad function and its role in transcription of Smad7 were investigated in cotransfection experiments using Smad7 promoter-luciferase reporter construct containing the sequence between -408 bp and +112 bp of mouse Smad7 gene. The data were analysed by one-way ANOVA.
RESULTS
When the Smad7 promoter-luciferase reporter gene construct was expressed in MDPC-23 cells, its transcriptional activity was significantly induced by TGF-beta1 treatment, whereas not by BMP-2 treatment. Overexpression of Smad1, 2, 4, or 5 had no effect on transcriptional activity of Smad7 promoter. Overexpression of Smad3 markedly promoted transcriptional activity of Smad7 promoter, whereas co-transfection of Smad3 and Smad4 doubled the effect of Smad3. Overexpression of Smad3 dominant negative mutant or Smad3 antisense cDNA (AS-Smad3) significantly inhibited transcriptional activity of Smad7 promoter induced by TGF-beta1.
CONCLUSION
TGF-beta1 regulated transcription of Smad7 gene through association of Smad3 and Smad4 in MDPC-23 cells.
目的
研究Smad信号在转化生长因子-β1（TGF-β1）介导的成牙本质细胞系MDPC-23中Smad7基因转录中的作用，探讨TGF-β1在转录水平介导Smad7基因表达的分子机制。
方法
使用包含小鼠Smad7基因-408 bp至+112 bp序列的Smad7启动子-荧光素酶报告基因构建体，通过共转染实验研究Smad功能及其在Smad7转录中的作用。数据采用单因素方差分析。
结果
当Smad7启动子-荧光素酶报告基因构建体在MDPC-23细胞中表达时，TGF-β1处理可显著诱导其转录活性，而骨形态发生蛋白-2（BMP-2）处理则无此作用。Smad1、2、4或5的过表达对Smad7启动子的转录活性无影响。Smad3的过表达显著促进Smad7启动子的转录活性，而Smad3和Smad4共转染可使Smad3的作用增强一倍。Smad3显性负突变体或Smad3反义cDNA（AS-Smad3）的过表达显著抑制TGF-β1诱导的Smad7启动子的转录活性。
结论
在MDPC-23细胞中，TGF-β1通过Smad3和Smad4的结合调节Smad7基因的转录。
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