Zinc balance is critical for NFI-C mediated regulation of odontoblast differentiation.

Zinc is trace element essential for diverse metabolic and cellular signaling pathways for the growth, development, and maintenance. Zinc deficiency is involved in bone malformations and oral disease. Mice deficient in zinc transporter Zip13 show connective tissue and skeletal disorders, abnormal incisor teeth, and reduced root dentin formation in the molar teeth and share a morphologically similar phenotype to nuclear factor I-C (NFI-C)-deficient mice.

Odontogenic ameloblasts-associated protein (ODAM), via phosphorylation by bone morphogenetic protein receptor type IB (BMPR-IB), is implicated in ameloblast differentiation.

To elucidate the function of the odontogenic ameloblast-associated protein (ODAM) in ameloblasts, we identified more than 74 proteins that interact with ODAM using protoarray. Of the identified proteins, bone morphogenetic protein receptor type-IB (BMPR-IB) was physiologically relevant in differentiating ameloblasts. ODAM and BMPR-IB exhibited similar patterns of expression in vitro, during ameloblast differentiation.

Crosstalk between nuclear factor I-C and transforming growth factor-β1 signaling regulates odontoblast differentiation and homeostasis.

Transforming growth factor-β1 (TGF-β1) signaling plays a key role in vertebrate development, homeostasis, and disease. Nuclear factor I-C (NFI-C) has been implicated in TGF-β1 signaling, extracellular matrix gene transcription, and tooth root development. However, the functional relationship between NFI-C and TGF-β1 signaling remains uncharacterized.

The odontogenic ameloblast-associated protein (ODAM) cooperates with RUNX2 and modulates enamel mineralization via regulation of MMP-20.

We have previously reported that the odontogenic ameloblast-associated protein (ODAM) plays important roles in enamel mineralization through the regulation of matrix metalloproteinase-20 (MMP-20). However, the precise function of ODAM in MMP-20 regulation remains largely unknown. The aim of the present study was to uncover the molecular mechanisms responsible for MMP-20 regulation.

Nuclear factor I-C is essential for odontogenic cell proliferation and odontoblast differentiation during tooth root development.

Our previous studies have demonstrated that nuclear factor I-C (NFI-C) null mice developed short molar roots that contain aberrant odontoblasts and abnormal dentin formation. Based on these findings, we performed studies to elucidate the function of NFI-C in odontoblasts. Initial studies demonstrated that aberrant odontoblasts become dissociated and trapped in an osteodentin-like mineralized tissue.

Disruption of Nfic causes dissociation of odontoblasts by interfering with the formation of intercellular junctions and aberrant odontoblast differentiation.

We reported previously that Nfic-deficient mice exhibit short and abnormal molar roots and severely deformed incisors. The objective of this study is to address the mechanisms responsible for these changes using morphological, IHC, and RT-PCR analysis. Nfic-deficient mice exhibited aberrant odontoblasts and abnormal dentin formation in molar roots and the labial crown analog of incisors.

The effect of odontoblast conditioned media and dentin non-collagenous proteins on the differentiation and mineralization of cementoblasts in vitro.

Objective: Cementum is an important mineralized tissue in root formation, however, the precise mechanism of cementum formation remains undetermined. The purpose of this study was to evaluate the effect of odontoblast conditioned media (CM) and dentin non-collagenous proteins (dNCPs) on the differentiation and mineralization of cementoblastic OCCM-30 cells.

Methods: The CM of ameloblastic ALCs, odontoblastic MDPC-23 and OD-11, osteoblastic MG-63, and fibroblastic NIH3T3 cells were transferred to OCCM-30 cells.

Nfic gene disruption inhibits differentiation of odontoblasts responsible for root formation and results in formation of short and abnormal roots in mice.

Background: Nuclear factor I genes play an important role in the development of the brain, lung, and roots of teeth. We had reported that Nfic-deficient mice form normal crowns, but abnormal roots of molar teeth. However, the mechanism by which the disruption of Nfic gene causes abnormal root formation remains unknown.

The amyloid protein APin is highly expressed during enamel mineralization and maturation in rat incisors.

This study investigated the expression and localization of APin (which was previously identified and cloned from a rat odontoblast cDNA library), during ameloblast differentiation in rat incisors, by using in situ hybridization and immunohistochemistry. The subcellular localization of APin varied during ameloblast differentiation, but was stage-specific. APin mRNA was not expressed in pre-ameloblasts, was weakly expressed in secretory ameloblasts, and was strongly expressed in maturation-stage ameloblasts as well as in the junctional epithelium attached to the enamel of erupted molars.

Effect of dexamethasone on root resorption after delayed replantation of rat tooth.

The purpose of this study was to evaluate the effect of dexamethasone after delayed tooth replantation with specific regard to root resorption and ankylosis. In addition, the study was planned to elucidate further the usefulness of the model. Fifty-two maxillary first molar teeth were extracted from 26 Sprague-Dawley white female rats fed 0.

Essential role for NFI-C/CTF transcription-replication factor in tooth root development.

The mammalian tooth forms by a series of reciprocal epithelial-mesenchymal interactions. Although several signaling pathways and transcription factors have been implicated in regulating molar crown development, relatively little is known about the regulation of root development. Four genes encoding nuclear factor I (NFI) transcription-replication proteins are present in the mouse genome: Nfia, Nfib, Nfic, and NFIX: In order to elucidate its physiological role(s), we disrupted the Nfic gene in mice.