BMP2-induced gene profiling in dental epithelial cell line

Tooth development is regulated by epithelial-mesenchymal interactions and their reciprocal molecular signaling. Bone morphogenetic protein 2 (BMP2) is known as one of the inducers for tooth development. To analyze the molecular mechanisms of BMP2 on ameloblast differentiation (amelogenesis), we perf...

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Published inThe Journal of Medical Investigation Vol. 55; no. 3,4; pp. 216 - 226
Main Authors Harada, Hidemitsu, Miyoshi, Keiko, Nagata, Hideya, Horiguchi, Taigo, Abe, Kaori, Wahyudi, Ivan Arie, Noma, Takafumi, Baba, Yoshinobu
Format Journal Article
LanguageEnglish
Published Japan The University of Tokushima Faculty of Medicine 01.08.2008
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ISSN1343-1420
1349-6867
DOI10.2152/jmi.55.216

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Summary:Tooth development is regulated by epithelial-mesenchymal interactions and their reciprocal molecular signaling. Bone morphogenetic protein 2 (BMP2) is known as one of the inducers for tooth development. To analyze the molecular mechanisms of BMP2 on ameloblast differentiation (amelogenesis), we performed microarray analyses using rat dental epithelial cell line, HAT-7. After confirming that BMP2 could activate the canonical BMP-Smads signaling in HAT-7 cells, we analyzed the effects of BMP2 on 14,815 gene expressions and profiled them. Seventy-three genes were up-regulated and 28 genes were down-regulated by BMP2 treatment for 24 hours in HAT-7 cells. Functional classification revealed that 18% of up-regulated genes were ECM/adhesion molecules present in the enamel organ. Furthermore, we examined the expression of several differentiation markers in dental epithelial four cell-lineages including inner enamel epithelium (ameloblasts), stratum intermedium, stratum reticulum, and outer enamel epithelium. The results indicated that BMP2 might induce at least two different cell-lineage markers including a BMP antagonist expressed in HAT-7 cells, suggesting that BMP2 could accelerate amelogenesis via BMP signaling. J. Med. Invest. 55: 216-226, August, 2008
ISSN:1343-1420
1349-6867
DOI:10.2152/jmi.55.216