Analysis of murine hypophosphatasia using osteoblasts derived from dental pulp stem cells
Project/Area Number |
16K20658
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Orthodontics/Pediatric dentistry
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Research Institution | Nihon University |
Principal Investigator |
NEMOTO Seiko 日本大学, 松戸歯学部, 助教 (10633943)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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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 / 石灰化不全 |
Outline of Final Research Achievements |
Hypophosphatasia(HPP) is caused by mutation of the gene encoding tissue non-specific alkaline phosphatase (TNALP). Physiological function of TNALP has been investigated for years nevertheless the cellular mechanisms affecting calcification remain unclear. In this study we elucidated the bone metabolism of HPP model mice by bone morphomety to evaluate influence TNALP in the cells involving ossification. The osteoblasts decreased significantly in KO mice. In regard to the osteoclasts there were no differences. Trabecular bone width and bone volume / tissue volume of KO mice showed significant decrease in KO mice. Thinning of hypertrophic chondrocytes layer was shown in KO mice though the thick chondrocytes layer observed. These results indicate that TNALP effects the cell number of osteoblast and chondrocyte layer in KO mice. Therefore the lack of TNALP causes retarded bone mineralization in the HPP model mice.
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Report
(3 results)
Research Products
(6 results)