| Project/Area Number |
22590291
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
MIZUNO Atsuko 自治医科大学, 医学部, 助教 (30364532)
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| Co-Investigator(Kenkyū-buntansha) |
AMANO Hitoshi 昭和大学, 歯学部, 准教授 (90212571)
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| Project Period (FY) |
2010-04-01 – 2013-03-31
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 分子病態学 / 軟骨 / 分子病態 / 生体分子 / メカニカルストレス / 再生医学 |
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| Outline of Final Research Achievements |
TRPV4 (transient receptor potential vanilloid 4) is a Ca^<2+>-permeable cation channel activated by mechanical stimuli, and the gene is expressing in chondrocytes. Mtap7d1, a novel molecule isolated as possibly association with TRPV4, is also expressing in chondrocytes. To elucidate their function, we examined the skeletal structure and the growth plate chondrocytes in the gene deficient mice, TRPV4-KO and Mtap7d1-KO. TRPV4-KO showed the short tails due to shortened caudal vertebrae and partial defects in spatial arrangement of chondrocytes in the growth plate. Mtap7d1-KO newborns showed moderate achondroplasia and disorderd chondrocyte column in the growth plate. These results indicate that TRPV4 and Mtap7d1 play essential roles in development and orientation of chondrocytes in the growth plate during bone formation.
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