Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김계성 | - |
dc.date.accessioned | 2018-04-16T04:02:27Z | - |
dc.date.available | 2018-04-16T04:02:27Z | - |
dc.date.issued | 2012-01 | - |
dc.identifier.citation | Histochemistry and Cell Biology, 2012, 137(1), P.67~78 | en_US |
dc.identifier.issn | 0948-6143 | - |
dc.identifier.uri | https://link.springer.com/article/10.1007%2Fs00418-011-0876-1 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11754/67740 | - |
dc.description.abstract | Various cellular and molecular events are involved in palatogenesis, including apoptosis, epithelial–mesenchymal transition (EMT), cell proliferation, and cell migration. Smad2 and Snail, which are well-known key mediators of the transforming growth factor beta (Tgf-β) pathway, play a crucial role in the regulation of palate development. Regulatory effects of microRNA 200b (miR-200b) on Smad2 and Snail in palatogenesis have not yet been elucidated. The aim of this study is to determine the relationship between palate development regulators miR-200b and Tgf-β-mediated genes. Expression of miR-200b, E-cadherin, Smad2, and Snail was detected in the mesenchyme of the mouse palate, while miR-200b was expressed in the medial edge epithelium (MEE) and palatal mesenchyme. After the contact of palatal shelves, miR-200b was no longer expressed in the mesenchyme around the fusion region. The binding activity of miR-200b to both Smad2 and Snail was examined using a luciferase assay. MiR-200b directly targeted Smad2 and Snail at both cellular and molecular levels. The function of miR-200b was determined by overexpression via a lentiviral vector in the palatal shelves. Ectopic expression of miR-200b resulted in suppression of these Tgf-β-mediated regulators and changes of apoptosis and cell proliferation in the palatal fusion region. These results suggest that miR-200b plays a crucial role in regulating the Smad2, Snail, and in apoptosis during palatogenesis by acting as a direct non-coding, influencing factor. Furthermore, the molecular interactions between miR-200b and Tgf-β signaling are important for proper palatogenesis and especially for palate fusion. Elucidating the mechanism of palatogenesis may aid the design of effective gene-based therapies for the treatment of congenital cleft palate. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Verlag | en_US |
dc.subject | Palatogenesis | en_US |
dc.subject | MiR-200b | en_US |
dc.subject | Smad2 | en_US |
dc.subject | Snail | en_US |
dc.subject | Apoptosis | en_US |
dc.subject | Cell proliferation | en_US |
dc.title | MiR-200b is involved in Tgf-beta signaling to regulate mammalian palate development | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 137 | - |
dc.identifier.doi | 10.1007/s00418-011-0876-1 | - |
dc.relation.page | 67-78 | - |
dc.relation.journal | HISTOCHEMISTRY AND CELL BIOLOGY | - |
dc.contributor.googleauthor | Jeong-Oh, Shin | - |
dc.contributor.googleauthor | Jong-Min, Lee | - |
dc.contributor.googleauthor | Kyoung-Won, Cho | - |
dc.contributor.googleauthor | Sungwook, Kwak | - |
dc.contributor.googleauthor | Hyuk-Jae, Kwon | - |
dc.contributor.googleauthor | Min-Jung, Lee | - |
dc.contributor.googleauthor | Sung-Won, Cho | - |
dc.contributor.googleauthor | Kye-Seong, Kim | - |
dc.contributor.googleauthor | Han-Sung, Jung | - |
dc.relation.code | 2012203665 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | ks66kim | - |
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