| Project/Area Number |
16592055
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Orthodontic/Pediatric dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
NAKAJIMA Akira Nihon University, School of Dentistry, Assistant, 歯学部, 助手 (50297842)
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| Co-Investigator(Kenkyū-buntansha) |
ISOKAWA Keitaro Nihon University, School of Dentistry, Professor, 歯学部, 教授 (50168283)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | secondary palatal fusion / epithelial-mesenchymal cells / Medial edge of epithelium / cleft palate / development / Mesial edge of epithelium / plaltal fusion / trandforming growth factor / epithelial / mesenchyme / transformation |
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| Research Abstract |
The medial edge epithelium has an important role in the fusion of the secondary palate. A multi-layer epithelial seam is formed by the adhesion of the two opposing medial edge epithelia (MEE) covering the tips of the palatal shelves at E14 in the mouse. Thereafter the MEE seam thins to a single cell layer at E14.5, while at the same time MEE cells accumulate at the oral and nasal sides to form epithelial triangles. The epithelial seam eventually disappears so that only mesenchyme cells are observed in the midline of the palate, with epithelial remnants absent by E15.
The fate of MEE has been attributed to three different mechanisms. A programmed cell death (PCD) fate for the MEE was hypothesized for many years. An epithelial-mesenchymal transdifferentiation (EMT) fate for the MEE has been demonstrated more recently. Additionally some MEE retain their epithelial phenotype and migrate to merge with the nasal and oral surface epithelia.
We have used the two-component Wnt1-Cre/R26R model to mark the cranial neural crest cell (CNC) derived mesenchyme in the secondary palate. This model has permitted the identification of non-CNC-derived palatal mesenchymal cells. Mesenchymal cells derived from transdifferentiated MEE will not express ?-gal and thus this marker could potentially aid in the identification of MEE-derived cells following palatal fusion.
This present in vivo and in vitro study has been completed to determine if the use of both heritable markers and cell lineage dyes would permit the identification of transdifferentiated MEE and allow characterization of the persistence of MEE-specific expression of TGF-?3 and T?R-III in these mesenchymal cells.
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