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The Epithelial-Mesenchymal Interaction Plays a Role in the Maintenance of the Stem Cell Niche of Mouse Incisors via Fgf10 and Fgf9 Signaling



Tamaki Yokohama-Tamaki1, Naoki Fujiwara2, Shunichi Shibata1, Satoshi Wakisaka3, Hidemitsu Harada2, *
1 Division of Histology, Department of Oral Growth and Development, School of Dentistry, Health Sciences University of Hokkaido, Hokkaido, Japan
2 Department of Oral Anatomy II, School of Dentistry, Iwate Medical University, Iwate, Japan and
3 Department of Oral Anatomy and Developmental Biology, Graduate School of Dentistry, Osaka University, Osaka, Japan


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© 2008 Yokohama-Tamaki et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

* Address correspondence to this author at the Department of Oral Anatomy II, School of Dentistry, Iwate Medical University, Iwate, Japan 020-8505, Japan; Tel: +81-19-651-5111; Fax: +81-19-652-4652; E-mail: hideha@iwate-med.ac.jp


Abstract

The continuous eruption of mouse incisors throughout life is maintained by adult stem cells in the apical end. In these teeth, the continuous expression of Fgf10 in the mesenchyme plays a role in the maintenance of the epithelial stem cell compartment, referred to as the "apical bud." However, little is known about the epithelial signaling that induces and maintains Fgf10 expression. Focusing on the epithelial-mesenchymal interaction during tooth development, we thoroughly investigated candidates expressed in the apical bud. In situ hybridization and immunostaining showed that Fgf9 mRNA and protein were detected in the basal epithelium, stellate reticulum, and inner enamel epithelium of the apical bud. Recombinant Fgf9 protein stimulated cell proliferation in cultures of apical end mesenchyme. Furthermore, Fgf9- releasing beads inhibited apoptosis in mesenchymal tissue cultures and maintained the expression of Fgf10. On the other hand, Fgf10-releasing beads induced Fgf9 expression in cultures of apical buds. Taken together, these results suggest that the stem cell niche in growing incisors is maintained by an epithelial mesenchymal interaction via Fgf9 and Fgf10 signaling.