| Project/Area Number |
15390638
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | KYUSHU UNIVERSITY |
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Principal Investigator |
NONAKA Kazuaki Kyushu University, Faculty of Dental Science, Professor, 大学院・歯学研究院, 教授 (90128067)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUTI Noboru Kyushu University, Faculty of Dental Science, Research Associate, 大学院・歯学研究院, 助手 (00230368)
IIDA Hiroshi Kyushu University, Faculty of Agriculture, Associate Professor, 大学院・農学研究院, 助教授 (70150399)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 2004: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2003: ¥3,600,000 (Direct Cost: ¥3,600,000)
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| Keywords | Maternal Effect / Amnio Fluid / Cleft lip / Cleft Palate / CL / Fv Mouse / Fusion / Molecular Event / TGF-beta3 / 口唇裂口蓋裂自然発症CL / Frマウス / 血管新生 / 組織癒合 / 歯の発育 / 頚顔面頭蓋発育 / 口唇裂 / 口唇癒合 / CL / TGF-β3 / 分子機序 |
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| Research Abstract |
TGF-b3 mediates epithelial-mesenchymal transformation during normal fusion of lip and palate, but how TGF-b3 functions during cleft lip repair remains unexplored. We hypothesize that TGF-b3 promotes fetal cleft lip repair and fusion by increasing the availability of nesenchymal cells. In this investigation, we demonstrated that cleft lips in mouse fetuses were repaired by fetal surgery, producing scarless fusion. At the site of the operation, we first observed an infusion of platelet expressing TGF-b3, followed by increased expression of cyclin D1 and tenascin-C, and coupled with increased mesenchymal cell proliferation. In an ex vivo serumless culture system, cleft lip explants fused in the presence of exogenous TGF-b3. Cultured lips also showed up-regulation in cyclin D1 and tenascin-C expression. These findings suggest that microsurgical repair of cleft lip in the fetus that produced scarless fusion is mediated by TGF-b3 regulation of mesenchymal cell proliferation and migration at the site of repair.
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