Nuclear factor I-C (NFI-C) null mice demonstrated aberrant odontoblast differentiation, abnormal dentin formation, and thus molar lacking roots. However, the mechanism by which the disruption of NFI-C gene affect the expression of other genes in dental pulp cells remains unknown. In this study, in order to understand this mechanism, the gene expression of pulp cells in NFI-C deficient mice were compared to those of wild-type mice by cDNA microarray analysis. According to the cDNA microarray profile comparison, the disruption of NFI-C gene increased the expression of TGF-β and TGF-β receptor, whereas it decreased the expression of Smad proteins. Interestingly, most of the FGF-related genes were down-regulated in pulp cells by NFI-C gene disruption. Among the cell cycle-related genes, the expression of p16 and p18 were increased by NFI-C disruption, but the expression of cy clin E1 and cy clin D1 were decreased by NFI-C disruption. These results indicate that the disturbance of NFI-C gene suppressed the proliferation of pulp cells and up-regulated the expression of TGF-β and its downstream signaling molecules during root formation, contributing to the formation of short root containing abnormal dentin.

Nuclear factor 1 (NFI) was discovered as a protein required for adenovirus DNA replication in vitro, but it is now clear that NFI protein plays an important role in the expression of many cellular genes. NFI-C null mice demonstrated aberrant odontoblast differentiation, abnormal dentin formation, and thus molar lacking roots while other tissues/or gans in the body, including ameloblasts appear to be unaffected and normal. However, little is known about the mechanism of NFI -C function in odontoblast differentiation and dentin formation. In this study, in order to elucidate the molecular mechanisms of odntoblast differentiation, we examined morphological characteristics of the aberrant odontoblast in NFI-C null mice. we also evaluate the expression of dentin sialophosphoprotein (DSPP) and bone sialoprotein (BSP) mRNAs in the MDPC-23 cells by northern analysis after over-expression and inactiγation of NFI -C into mouse MDPC-23 cells Odontoblasts of the NFI-C null mouse were round in shape, lost their polarity, organized as a sheet of cells, and trapped in osteodentin-like mineralized tissue. Abnormal odontoblasts of NFI-C null mouse revealed the absence of an intercellular junctional complex known as the t erminal webs. MDPC-23 cells started to express DSPP mRNA beginning from the postnatal day of 14 and showed a steady increase as differentiating into odontoblasts. Over-expression of NFI -C increased the expression of DSPP mRNA. Inactivation of NFI - C induced BSP mRNA expression. These results suggest that NFI-C plays an important role in odontoblast differentiation in a cell-type specific manner and thus in dentin formation