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  Follistatin antagonizes transforming growth factor-β3-induced epithelial–mesenchymal transition in vitro: implications for murine palatal development supported by microarray analysis

Nogai, H., Rosowski, M., Grün, J., Rietz, A., Debus, N., Schmidt, G., Lauster, C., Janitz, M., Vortkamp, A., & Lauster, R. (2008). Follistatin antagonizes transforming growth factor-β3-induced epithelial–mesenchymal transition in vitro: implications for murine palatal development supported by microarray analysis. Differentiation, 76(4), 404-416. doi:10.1111/j.1432-0436.2007.00223.x.

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資料種別: 学術論文

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 作成者:
Nogai, Hendrik, 著者
Rosowski, Mark, 著者
Grün, Joachim, 著者
Rietz, Anika, 著者
Debus, Nils, 著者
Schmidt, Gül, 著者
Lauster, Carola, 著者
Janitz, Michal1, 著者           
Vortkamp, Andrea2, 著者           
Lauster, Roland, 著者
所属:
1Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433550              
2Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433554              

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キーワード: Cleft palate, Palatal fusion, EMT, TGF-β, Follistatin
 要旨: Abstract Epithelial–mesenchymal transition (EMT) is involved in normal embryonic development as well as in tumor progression and invasiveness. This process is also known to be a crucial step in palatogenesis during fusion of the bi-lateral palatal processes. Disruption of this step results in a cleft palate, which is among the most frequent birth defects in humans. A number of genes and encoded proteins have been shown to play a role in this developmental stage. The central role is attributed to the cytokine transforming growth factor-β3 (TGF-β3), which is expressed in the medial edge epithelium (MEE) already before the fusion process. The MEE covers the tips of the growing palatal shelves and eventually undergoes EMT or programmed cell death (apoptosis). TGF-β3 is described to induce EMT in embryonic palates. With regard to the early expression of this molecule before the fusion process, it is not well understood which mechanisms prevent the TGF-β3 producing epithelial cells from undergoing differentiation precociously. We used the murine palatal fusion to study the regulation of EMT. Specifically, we analyzed the MEE for the expression of known antagonists of TGF-β molecules using in situ hybridization and detected the gene coding for Follistatin to be co-expressed with TGF-β3. Further, we could show that Follistatin directly binds to TGF-β3 and that it completely blocks TGF-β3-induced EMT of the normal murine mammary gland (NMuMG) epithelial cell line in vitro. In addition, we analyzed the gene expression profile of NMuMG cells during TGF-β3-induced EMT by microarray hybridization, detecting strong changes in the expression of apoptosis-regulating genes.

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言語: eng - English
 日付: 2008-04
 出版の状態: 出版
 ページ: -
 出版情報: -
 目次: -
 査読: -
 学位: -

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出版物名: Differentiation
種別: 学術雑誌
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出版社, 出版地: -
ページ: - 巻号: 76 (4) 通巻号: - 開始・終了ページ: 404 - 416 識別子(ISBN, ISSN, DOIなど): ISSN: 0301-4681