| Project/Area Number |
24249093
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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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 | Osaka University (2013-2014)
Okayama University (2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
川邉 紀章 岡山大学, 医歯(薬)学総合研究科, 准教授 (00397879)
村上 隆 岡山大学, 大学病院, 講師 (00534786)
伊藤 慎将 大阪大学, 歯学研究科(研究院), 助教 (40633706)
上岡 寛 岡山大学, 医歯(薬)学総合研究科, 教授 (80253219)
柳田 剛志 岡山大学, 大学病院, 講師 (90534793)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAGAWA ICHIRO 京都大学, 医学研究科, 教授 (70294113)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥45,240,000 (Direct Cost: ¥34,800,000、Indirect Cost: ¥10,440,000)
Fiscal Year 2014: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2013: ¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2012: ¥21,710,000 (Direct Cost: ¥16,700,000、Indirect Cost: ¥5,010,000)
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| Keywords | Runxシグナリング / 上皮間葉相互作用 / 器官形成 / Cbfb / Runx1 / 唾液腺 / 歯 / 皮膚付属器官 / Ｃｂｆｂ / 切歯 / 臼歯 |
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| Outline of Final Research Achievements |
In this study, we investigated the possible roles of epithelial Runx1/Cbfb signaling in the organogenesis and craniofacial development. Using the epithelial-specific Runx1 knock-out and epithelial-specific Cfbf knock-out mice, we provided evidence that Runx1/Cbfb has indispensable roles in the development of the teeth, the salivary gland, and the palate. In salivary gland, Runx1 is involved in sexual dimorphism in the induction of the granular convoluted tubules of the submandibular gland in the presence of androgen. In the incisors, Runx1 is involved in the regulation of Lgr5-positive epithelial stem cells that differentiate into ameloblasts, through regulation of phosphorylation of Stat3 in the cervical loop of the growing incisors. In the palate, Runx1 epithelial-specific deletion led to the failed disintegration of the contacting palatal epithelium and that Tgfb3 is a critical downstream target in the pathogenesis of anterior cleft palate in the mutants.
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