| Project/Area Number |
26462825
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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 |
Functional basic dentistry
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| Research Institution | Tsurumi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
二藤 彰 鶴見大学, 歯学部, 教授 (00240747)
和田 悟史 鶴見大学, 歯学部, 助教 (20581119)
山下 照仁 松本歯科大学, 総合歯科医学研究所, 准教授 (90302893)
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| Research Collaborator |
ARAI Yoshinori
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | Annexin a5 / 腱 / 靭帯 / 骨 / アネキシンA5 |
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| Outline of Final Research Achievements |
Entheses can be further divided to fibrocartilaginous and fibrous entheses according to the type of tissue present at the skeletal attachment site. In Anxa5-deficient (Anxa5-/-) mice, the sizes of bone ridge outgrowths at the fibrocartilaginous entheses of tibiae and femur were increased after 7 weeks of age. This bone overgrowth was not observed at the fibrous enthesis where Anxa5-lacZ is hardly expressed. At the fibrocartilaginous entheses, more ALP-expressing cells were observed in the fibrocartilage layer outside of the bone in the mutant mice. Then, to examine the role of Anxa5 on cartilage differentiation, we performed Anxa5 gene knockdown in vitro using siRNA. Depletion of endogenous Anxa5 with siRNA increased mRNA expressions of differentiated marker of chondrocyte. Together, these results suggest that Anxa5 prevents bone overgrowth at the fibrocartilaginous entheses.
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