| Project/Area Number |
21592482
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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 |
Prosthetic dentistry
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| Research Institution | Osaka Dental University |
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Principal Investigator |
INOUE Masahiro 大阪歯科大学, 歯学部・附属病院, 准教授 (50159993)
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| Co-Investigator(Kenkyū-buntansha) |
KUREMOTO Koh-ichi 広島大学, 大学院・医歯薬学総合研究科, 助教 (90319583)
MAEDA Teruta 大阪歯科大学, 歯学部・附属病院, 教授 (10103110)
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| Co-Investigator(Renkei-kenkyūsha) |
YAMAZA Takayoshi 九州大学, 歯学部, 助教 (80304814)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | FGF / 口腔上皮 / 幹細胞 / 粘膜再生 |
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| Research Abstract |
Fibroblast growth factor-10(FGF-10) is a known epithelial mitogen in several organ systems, such as the lung, that acts in a bidirectional paracrine manner and acts exclusively through a subset of receptors such as FGFr2b. However, its role in oral epithelial regeneration is unknown. We investigated the role of FGFr2b/FGF-10 signaling in oral epithelial wound healing using FGF-10 overexpression(OE) and FGFr2b attenuation/knock-down(KD) transgenic mice. The present results suggested that, 1) Under-developing of the epithelial layer was noted in the FGFr2b KD mice, whereas over-developing was noted in the FGF-10 OE mice. 2) FGF10 overexpression initiated the parakeratosis of oral epithelium or urothelium and 3) FGF10 overexpression worked the proliferation of the basal laminae in the stratified squamous epithelium and transitional epithelium. Form these results, FGF-10/FGFr2b signaling appears to play an active proliferation in Oral Epithelial Stem Cells, and accelerate the regenerative capacity of the oral epithelium.
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