Nuclear Factor I-C (NFIC) Regulates Dentin Sialophosphoprotein (DSPP) and E-cadherin via Control of Krüppel-like Factor 4 (KLF4) During Dentinogenesis
| Autor: | Joo-Cheol Park, Kwang-Hee Cho, Hye Kyung Lee, Su-Jin Park, Hyun-Sook Bae, Dong-Seol Lee |
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| Rok vydání: | 2014 |
| Předmět: |
Transcription
Genetic Sialoglycoproteins Cellular differentiation Kruppel-Like Transcription Factors Odontoblast differentiation Biochemistry Kruppel-Like Factor 4 Mice stomatognathic system Dentin sialophosphoprotein Genes Reporter Ameloblasts Animals Humans Luciferases Promoter Regions Genetic Molecular Biology Mice Knockout Extracellular Matrix Proteins Odontoblasts Chemistry fungi Gene Expression Regulation Developmental Cell Differentiation Cell Biology Anatomy Dentinogenesis Cadherins Phosphoproteins DMP1 Rats Cell biology NFI Transcription Factors stomatognathic diseases HEK293 Cells Odontoblast NFIC Dentin embryonic structures Pulp (tooth) sense organs Protein Binding Signal Transduction |
| Zdroj: | Journal of Biological Chemistry. 289:28225-28236 |
| ISSN: | 0021-9258 |
| DOI: | 10.1074/jbc.m114.568691 |
| Popis: | Odontoblasts are a type of terminally differentiated matrix-secreting cells. A number of molecular mechanisms are involved in the differentiation of odontoblasts. Several studies demonstrated that Krüppel-like factor 4 (KLF4) promotes odontoblast differentiation via control of dentin sialophosphoprotein (DSPP). Because nuclear factor I-C (NFIC) is also known to control DSPP, we investigated the relationship between NFIC and KLF4 during odontoblast differentiation. Klf4 mRNA expression was significantly decreased in Nfic(-/-) pulp cells compared with wild type cells. In immunohistochemistry assays, dentin matrix protein 1 (Dmp1), and DSP protein expression was barely observed in Nfic(-/-) odontoblasts and dentin matrix. Nfic bound directly to the Klf4 promoter and stimulated Klf4 transcriptional activity, thereby regulating Dmp1 and DSPP expression during odontoblast differentiation. Nfic or Klf4 overexpression promoted mineralized nodule formation in MDPC-23 cells. In addition, Nfic overexpression also decreased Slug luciferase activity but augmented E-cadherin promoter activity via up-regulation of Klf4 in odontoblasts. Our study reveals important signaling pathways during dentinogenesis: the Nfic-Klf4-Dmp1-Dspp and the Nfic-Klf4-E-cadherin pathways in odontoblasts. Our results indicate the important role of NFIC in regulating KLF4 during dentinogenesis. |
| Databáze: | OpenAIRE |
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