1999 Fiscal Year Final Research Report Summary
Molecular mechanisms of cleft palate formation in knockout mice
| Project/Area Number |
10671723
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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 |
Morphological basic dentistry
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| Research Institution | The Nippon Dental University |
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Principal Investigator |
TAYA Yuji The Nippon Dental University, School of Dentistry at Tokyo, Department of Pathology, Lecturer, 歯学部, 講師 (30197587)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMAZU Yoshihito The Nippon Dental University, School of Dentistry at Tokyo, Department of Pathology, Assistant Professor, 歯学部, 助手 (10297947)
SATO Kaori The Nippon Dental University, School of Dentistry at Tokyo, Department of Pathology, Assistant Professor, 歯学部, 助手 (90287772)
YAGISHITA Hisao The Nippon Dental University, School of Dentistry at Tokyo, Department of Pathology, Lecturer, 歯学部, 講師 (50256989)
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| Project Period (FY) |
1998 – 1999
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| Keywords | secondary palatogenesis / knockout mice / medial edge epithelium / deltaEF-1 / endothelin / cell adhesion / programmed cell death / proteoglycan |
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| Research Abstract |
Secondary palatogenesis in the mammal provides an excellent experimental model to investigate the mechanism of embryonal morphogenesis comprising cell proliferation and differentiation, and their movement and extinction at specified developmental stages. In the present work using mouse embryos (C57BL/6 and ICR), we focused our attention on the temporo-spatial changes in tissue organization composing of epithelial and messenchymal cells throughout palatogenesis. The critical event prior to completion of secondary palatogenesis required differentiation of the epithelial cell population into the medial edge epithelial (MEE) cells, which correspond to approximately 4,000 cells in a pair of the shelves. Filopodia on the MEE cell surface mediated an initial contact between the opposing shelves. After the cellular contact, the high mobility of MEE cells facilitated construction of the midline epithelial seam, which eventually became discontinuous and disappeared prior to mesenchymal confluenc
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e. Regarding the fate of the MEE cells at the midline position of mouse secondary palate, our results support the concomitant occurrence of programmed cell death at low frequencies, epithelial-mesenchymal transformation, and cell migration to join with oral or nasal epithelium. We also examined the structural changes and migration of MEE (medial edge epithelial) cell during the fusion of mouse embryonic palatal shelves in vitro. The palatal shelves used were prelabelled by CCFSE (carboxy-dichlorofluorescein diacetate succinimidyl ester) for 30 min at room temperature. The results obtained from the cultured shelves revealed that : (a) selective CCFSE- labeling was attained in the MEE cells, (b) a large number of the CCFSE-labeled MEE cells were clustered in the epithelial triangles, thereafter shedding into the cavities along the midline seam, and c only a few labeled cells at disintegrating seams appeared to merge into the mesenchymal cells. The overall results support the concept that the MEE cells are destined for discrete terminations during palatogenesis. Less
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