| Project/Area Number |
26293435
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthodontics/Pediatric dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IWAMOTO Tsutomu 徳島大学, 大学院医歯薬学研究部, 教授 (90346916)
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| Co-Investigator(Kenkyū-buntansha) |
長谷川 智一 徳島大学, 大学院医歯薬学研究部, 講師 (50274668)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2014: ¥10,140,000 (Direct Cost: ¥7,800,000、Indirect Cost: ¥2,340,000)
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| Keywords | 前象牙芽細胞 / Pannexin / Panx3 / ATP channel / AMPK / 象牙芽細胞 / 細胞増殖 / 細胞分化 / 歯の発生 / 細胞間結合 / パネキシン / ギャップ結合分子 |
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| Outline of Final Research Achievements |
The purpose of this study is to clarify the roles of preodontoblasts in tooth development. Here we have found that the expression of Panx3 was predominately localized in preo- dontoblasts that arise from dental papilla cells and can differentiate into dentin-secreting odontoblasts. Overexpression of Panx3 in dental mesenchymal cells reduced cell proliferation via up-regulation of p21, and promoted the BMP2-induced phosphorylation of Smad1/5/8 and the expression of Dspp, a marker of differentiated odontoblasts. Furthermore, Panx3 functions ATP release into the extracellular space through its hemichannel and induced the phosphorylation of AMPK. Our results suggest that Panx3 modulates intracellular ATP levels, resulting in the inhibition of odontoblast proliferation through the AMPK/p21 signaling pathway and promotion of cell differentiation by the BMP/Smad signaling pathway.
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