| Project/Area Number |
25862035
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Orthodontics/Pediatric dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
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| Research Collaborator |
YOKOI Eri
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | アルカリホスファターゼ / 低ホスファターゼ症 / 歯髄幹細胞 / 石灰化不全 / 幹細胞 / 歯髄 / 体性幹細胞 / 硬組織 |
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| Outline of Final Research Achievements |
Hypophospatasia (HPP) is caused by mutation of the gene tissue-nonspecific alkaline phosphatase (TNALP). TNALP is expressed in many tissues of the body. HPP have been various symptoms such as rickets, osteomalacia and dental manifestations. Dental symptoms are commonly shown in all types of HPP. However, cause of enamel defect is still unexplained. In this study, we compared between HPP model (KO) mice and wild type(WT) mice as control mice by microarray analysis using dental pulp stem cells. Microarray analysis revealed the genes related enamel development decreased in KO mice. Additionally, the gene expression levels of Amelx, Ambn and Enam in KO mice were lower than WT mice with RT-qPCR. Particularly, amount of Ambn and Enam significantly decreased (p<0.05). It is suggested that missing TNALP gene may affect to enamel defect in KO mice as the result of decreased the enamel matrix protein genes expression. Our study might help the elucidation in cause of enamel defects in human HPP.
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