Role of Smad signaling in transcription of Smad7 gene mediated by TGF-beta1 in odontoblast cell line MDPC-23
He, W.-x.; Niu, Z.-y.; Zhao, S.-l.; Zang, X.-x.; Gao, J.; Li, P.
Shanghai Kou Qiang Yi Xue 14(2): 143-146
2005
ISSN/ISBN: 1006-7248 PMID: 15886838 Document Number: 589471
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. 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. 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. TGF-beta1 regulated transcription of Smad7 gene through association of Smad3 and Smad4 in MDPC-23 cells.