アクセス数 : ?
ダウンロード数 : ?
ID 110844
著者
Ruspita, Intan Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School
三好, 圭子 Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
武藤, 太郎 Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School
阿部, 佳織 Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School KAKEN研究者をさがす
堀口, 大吾 Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
野間, 隆文 Department of Molecular Biology, Institute of Health Biosciences, The University of Tokushima Graduate School 徳島大学 教育研究者総覧 KAKEN研究者をさがす
キーワード
ameloblast
amelogenesis
follistatin
microarray
Sp
資料タイプ
学術雑誌論文
抄録
Sp6 is a member of the Sp family of transcription factors that regulate a wide range of cellular functions, such as cell growth and differentiation. Sp6, also called epiprofin, is specifically expressed in tooth germ, limb bud, and hair follicle, but there is little information on its function. To investigate the possible role of Sp6 in tooth development, first we established an Sp6- overproducing clone, CHA9, and analyzed the features of the cell, including cell proliferation and gene expression. The parental cells of CHA9 are the ameloblast-lineage G5 cells that we previously established from rat dental epithelia of lower incisor. Sp6 overproduction accelerated cell proliferation and induced the expression of ameloblastin mRNA, a marker of ameloblast differentiation. Second, we performed genome-wide screening of Sp6 target genes by microarray analysis. Out of a total 20,450 genes, 448 genes were up-regulated and 500 genes were down-regulated by Sp6. We found the expression of follistatin, a BMP antagonist, to be 22.4-fold lower in CHA9 than in control cells. Transfection of the Sp6-antisense construct into CHA9 cells restored follistatin expression back to equivalent levels seen in control cells, indicating that Sp6 regulates follistatin gene expression in ameloblasts. Our findings demonstrate that the follistatin gene is one of the Sp6 target genes in ameloblasts and suggest that Sp6 promotes amelogenesis through inhibition of follistatin gene expression.
掲載誌名
The journal of medical investigation : JMI
ISSN
13431420
cat書誌ID
AA11166929
55
1-2
開始ページ
87
終了ページ
98
並び順
87
発行日
2008-02
EDB ID
出版社版DOI
出版社版URL
フルテキストファイル
言語
eng
著者版フラグ
出版社版
部局
歯学系
病院