2014 Fiscal Year Final Research Report
Abnormal growth and causative factor in cartilage calcification insufficient rat
| Project/Area Number |
24592789
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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) |
TANUMA Jun-ichi 朝日大学, 歯学部, 教授 (20305139)
WATANABE Minoru 聖マリアンナ医科大学, 医学(系)研究科(研究院), 講師 (10191800)
TANAKA Masami 会津大学短期大学部, 食物栄養学科, 教授 (00171801)
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| Co-Investigator(Renkei-kenkyūsha) |
AMANO Hitoshi 大阪歯科大学, 歯学部, 准教授 (90212571)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 軟骨内骨化 / 頭蓋底軟骨結合 / 下顎頭軟骨 / Ihhシグナリング / in situ hybridization / Gli1 |
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| Outline of Final Research Achievements |
The cartilage calcification insufficient (CCI) rat derived from Sprague-Dawley (SD) rat, show spontaneous skeletal dwarfism associated with delay of endochondral ossification. In this study, CCI rats after two weeks later of birth showed abnormal synchondrosis including longitudinally wider length of intra-sphenoidal and spheno-occipital synchondrosis compared to the normal phenotype of SD wild type rats. Real time PCR and over expression of Smo and Gli1 mRNA expected association with Ihh by in situ hybridization, showed prominent relative increasing of transcription in CCI rats and this was supported by up-regulated BrdU incorporation. The data demonstrate CCI rats affect their endochondral ossification due to excessive Ihh signaling, results in hyper proliferating but feed-back arrest of chondrocyte differentiation in post-natal stage.
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| Free Research Field |
口腔病理学
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