Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts

Satoshi Fukumoto, Takayoshi Kiba, Bradford Hall, Noriyuki Iehara, Takashi Nakamura, Glenn Longenecker, Paul H. Krebsbach, Antonio Nanci, Ashok B. Kulkarni, Yoshihiko Yamada

研究成果: ジャーナルへの寄稿記事

252 引用 (Scopus)

抄録

Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

元の言語英語
ページ(範囲)973-983
ページ数11
ジャーナルJournal of Cell Biology
167
発行部数5
DOI
出版物ステータス出版済み - 12 5 2004

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Ameloblasts
Cell Adhesion Molecules
Tooth
Dental Enamel
Epithelium
Amelogenesis
Dental Enamel Hypoplasia
Odontogenic Tumors
Cell Polarity
Dentin
Morphogenesis
Epithelial Cells
Cell Proliferation
Phenotype

All Science Journal Classification (ASJC) codes

  • Cell Biology

これを引用

Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts. / Fukumoto, Satoshi; Kiba, Takayoshi; Hall, Bradford; Iehara, Noriyuki; Nakamura, Takashi; Longenecker, Glenn; Krebsbach, Paul H.; Nanci, Antonio; Kulkarni, Ashok B.; Yamada, Yoshihiko.

:: Journal of Cell Biology, 巻 167, 番号 5, 05.12.2004, p. 973-983.

研究成果: ジャーナルへの寄稿記事

Fukumoto, S, Kiba, T, Hall, B, Iehara, N, Nakamura, T, Longenecker, G, Krebsbach, PH, Nanci, A, Kulkarni, AB & Yamada, Y 2004, 'Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts', Journal of Cell Biology, 巻. 167, 番号 5, pp. 973-983. https://doi.org/10.1083/jcb.200409077
Fukumoto, Satoshi ; Kiba, Takayoshi ; Hall, Bradford ; Iehara, Noriyuki ; Nakamura, Takashi ; Longenecker, Glenn ; Krebsbach, Paul H. ; Nanci, Antonio ; Kulkarni, Ashok B. ; Yamada, Yoshihiko. / Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts. :: Journal of Cell Biology. 2004 ; 巻 167, 番号 5. pp. 973-983.
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abstract = "Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.",
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AU - Fukumoto, Satoshi

AU - Kiba, Takayoshi

AU - Hall, Bradford

AU - Iehara, Noriyuki

AU - Nakamura, Takashi

AU - Longenecker, Glenn

AU - Krebsbach, Paul H.

AU - Nanci, Antonio

AU - Kulkarni, Ashok B.

AU - Yamada, Yoshihiko

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N2 - Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

AB - Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin-null mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

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