| Project/Area Number |
22791396
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Keio University |
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Principal Investigator |
HOSHI Hiroko 慶應義塾大学, 医学部, 特任助教 (50399812)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 骨・軟骨代謝学 / アルコール分解酵素 / 骨代謝 / 骨粗鬆症 / 骨芽細胞 / 過酸化脂質 / アセトアルデヒド |
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| Research Abstract |
About half of the Japanese have a mutant ALDH2 gene, resulting to sensitivity to alcohol. In statistical analysis report, a mutation of the ALDH2 gene accelerates osteoporosis. However, the mechanism on how the mutated gene ALDH2 affects bone formation is still unknown. In this study, I try to work out the relation between the mutation of the ALDH2 gene and bone homeostasis by utilizing inactive ALDH2(ALDH2-DAL) mice. ALDH2-DAL mice exhibited osteoporosis and showed significantly reduced bone density. In morphometrical analysis, ALDH2-DAL trabecular and cortical bone thickness were thinner, and bone formation and mineralized rates were also decreased compared to that of wild type mice. Osteoblast in mice with mutated ALDH2 gene remarkably decreased compared to wild type osteoblasts by cell staining. The expression of marker genes on osteoblast differentiation of mice with mutated ALDH2-DAL gene was decreased compared to wild type osteoblasts.
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