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.

Although it has been known that TGF-β1 acts as a crucial cofactor in osteoclast differentiation, its mode of action is still unclear. In the present study, we studied the effect of TGF-β1 on the differentiation of osteoclast depending on the developmental stages. Murine bone marrow cells were induced to differentiate into mature osteoclasts in the presence of receptor activator of NF-xβ ligand (RANKL) and macrophage colony stimulating factor (M-CSF). In the early stage of the differentiation TRAP(-) mononuclear precursor cells were obtained from nonadherent M-CSF dependent bone marrow cells, which further differentiated into mature osteoclasts. TGF-β1 stimulated osteoclast differentiation, which was stronger when cells were stimulated by TGF-β1 in the early stage than the later differentiation. TGF-β1 increased the expression of RANK and synergistically stimulated RANKL-induced activation of NF-xβ MAP kinase in TRAP(-) mononuclear precursor cells. These results suggest that activation of osteoclast differentiation by TGF-β1 may be ascribed to the both increased expression and activation of RANK in the osteoclast differentiation, especially in the early stage of differentiation.