TY - JOUR
T1 - Transcriptional regulation of the basic helix-loop-helix factor AmeloD during tooth development
AU - Al Thamin, Shahad
AU - Chiba, Yuta
AU - Yoshizaki, Keigo
AU - Tian, Tian
AU - Jia, Ling Ling
AU - Wang, Xin
AU - Saito, Kan
AU - Li, Jiyao
AU - Yamada, Aya
AU - Fukumoto, Satoshi
N1 - Funding Information:
This study was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant‐in‐Aid (17H01606 to S.F., 20K18747 to Y.C. and 18H03009 to K.S.), and a research fellowship from FUTOKU foundation to YC. We appreciate the technical assistance provided by DNAFORM (Yokohama, Japan) for the CAGE analysis. The C57BL/6N (B6N) mouse BAC clone was provided by RIKEN BRC through the National BioResource Project of the MEXT/AMED, Japan. We thank the Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer Tohoku University for providing the cell lines.
Funding Information:
This study was supported by the Japan Society for the Promotion of Science (JSPS) KAKENHI, Grant-in-Aid (17H01606 to S.F., 20K18747 to Y.C. and 18H03009 to K.S.), and a research fellowship from FUTOKU foundation to YC. We appreciate the technical assistance provided by DNAFORM (Yokohama, Japan) for the CAGE analysis. The C57BL/6N (B6N) mouse BAC clone was provided by RIKEN BRC through the National BioResource Project of the MEXT/AMED, Japan. We thank the Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer Tohoku University for providing the cell lines.
Publisher Copyright:
© 2021 Wiley Periodicals LLC
PY - 2021/11
Y1 - 2021/11
N2 - The epithelial-mesenchymal interactions are essential for the initiation and regulation of the development of teeth. Following the initiation of tooth development, numerous growth factors are secreted by the dental epithelium and mesenchyme that play critical roles in cellular differentiation. During tooth morphogenesis, the dental epithelial stem cells differentiate into several cell types, including inner enamel epithelial cells, which then differentiate into enamel matrix-secreting ameloblasts. Recently, we reported that the novel basic-helix-loop-helix transcription factor, AmeloD, is actively engaged in the development of teeth as a regulator of dental epithelial cell motility. However, the gene regulation mechanism of AmeloD is still unknown. In this study, we aimed to uncover the mechanisms regulating AmeloD expression during tooth development. By screening growth factors that are important in the early stages of tooth formation, we found that TGF-β1 induced AmeloD expression and ameloblast differentiation in the dental epithelial cell line, SF2. TGF-β1 phosphorylated ERK1/2 and Smad2/3 to induce AmeloD expression, whereas treatment with the MEK inhibitor, U0126, inhibited AmeloD induction. Promoter analysis of AmeloD revealed that the proximal promoter of AmeloD showed high activity in dental epithelial cell lines, which was enhanced following TGF-β1 stimulation. These results suggested that TGF-β1 activates AmeloD transcription via ERK1/2 phosphorylation. Our findings provide new insights into the mechanisms that govern tooth development.
AB - The epithelial-mesenchymal interactions are essential for the initiation and regulation of the development of teeth. Following the initiation of tooth development, numerous growth factors are secreted by the dental epithelium and mesenchyme that play critical roles in cellular differentiation. During tooth morphogenesis, the dental epithelial stem cells differentiate into several cell types, including inner enamel epithelial cells, which then differentiate into enamel matrix-secreting ameloblasts. Recently, we reported that the novel basic-helix-loop-helix transcription factor, AmeloD, is actively engaged in the development of teeth as a regulator of dental epithelial cell motility. However, the gene regulation mechanism of AmeloD is still unknown. In this study, we aimed to uncover the mechanisms regulating AmeloD expression during tooth development. By screening growth factors that are important in the early stages of tooth formation, we found that TGF-β1 induced AmeloD expression and ameloblast differentiation in the dental epithelial cell line, SF2. TGF-β1 phosphorylated ERK1/2 and Smad2/3 to induce AmeloD expression, whereas treatment with the MEK inhibitor, U0126, inhibited AmeloD induction. Promoter analysis of AmeloD revealed that the proximal promoter of AmeloD showed high activity in dental epithelial cell lines, which was enhanced following TGF-β1 stimulation. These results suggested that TGF-β1 activates AmeloD transcription via ERK1/2 phosphorylation. Our findings provide new insights into the mechanisms that govern tooth development.
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U2 - 10.1002/jcp.30389
DO - 10.1002/jcp.30389
M3 - Article
C2 - 33844290
AN - SCOPUS:85104148632
VL - 236
SP - 7533
EP - 7543
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 0021-9541
IS - 11
ER -