| Project/Area Number |
17590255
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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 |
General medical chemistry
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| Research Institution | Jichi Medical University |
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Principal Investigator |
MIZUNO Atsuko Jichi Medical University, School of Medicine, Assistant, 医学部, 助手 (30364532)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Makoto Jichi Medical University, School of Medicine, Associate Professor, 医学部, 助教授 (10196868)
谷口 淳一 自治医科大学, 医学部, 講師 (90179838)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | cell tissue / regenerative medicine / biologic molecule |
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| Research Abstract |
[Objective]
TRPV4 channel is a calcium permeable cation channel which is activated by moderate heat, acidic pH and hypotonicity. TRPV4 may play as a mechanosensor on bone. To test this possibility, we compared the bone mass and chondrocytes, in TRPV4-/- mice and wild-type mice.
[Results]
1) RT-PCR and immunohistochemical analysis showed that mouse chondrocytes express TRPV4. 2) Electrophysiologic analysis revealed that the swell-activated cation current on chondrocyte induced by hypotonicity was absent in TRPV4-/- mice. 3) Detailed histological analysis showed that differentiation of chondrocytes in TRPV4-/- mice was slightly disordered. 4) Fracture healing model : there were no significant histological differences between TRPV4-/- and wild-type mice. 5) Primary cultured chondrocytes: expression patterns of collagen type X mRNA in TRPV4-/- mice were different from those in wild-type mice, by real-time PCR analysis.
[Conclusion]
TRPV4 channel functions as a mechanosensor sensing hypotonicity on the chondrocytes in mice. TRPV4 may act as a component molecule of the regulatory mechanism to response to mechanical stress in chondrocytes.
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