| Project/Area Number |
15K11030
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Asahi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
田沼 順一 朝日大学, 歯学部, 教授 (20305139)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 軟骨内骨化 / インディアンヘッジホッグ / 軟骨細胞 / 形態変化 / ヘッジホッグシグナル / 細胞増殖転写因子 / Gli1 / PTHrP / 下顎頭軟骨 / 頭蓋底軟骨 / Ihh |
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| Outline of Final Research Achievements |
The cartilage calcification insufficient (CCI) rat derived from Sprague-Dawley (SD) rat (permeability=25%), show spontaneous skeletal dwarfism associated with delay of endochondral ossification including craniofacial development, limbs pseudoarticulation and excurvature. In this study, CCI rats (2 weeks after birth) showed abnormal endchondral occification including longitudinally wider length of intra-sphenoidal and spheno-occipital synchondrosis, and exhibited morphological hypertrophic cartilage of mandibular condyle compared to the normal SD rats. Real time PCR for Gli1 gene showed prominent relative increasing of transcription in CCI rats. This dwarf is up-regulated BrdU incorporation, over expression of Ihh, Smo and Gli1 mRNA.
The data demonstrate that CCI rats affect their endochondral ossification due to excessive Ihh signaling, which results in hyper proliferating but feed-back arrest of chondrocyte differentiation to remain the layer of chondrocytes in post-natal development.
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