Analysis of molecular mechanism of Wnt signal and arachidonic acid cascade in intervertebral disc degeneration
| Project/Area Number |
26462252
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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 |
Orthopaedic surgery
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| Research Institution | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
酒井 大輔 東海大学, 医学部, 准教授 (10408007)
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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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腰痛 / 椎間板変性 / Wnt シグナル / PGE2 / TNF－α / 分子学的解析 / Wntシグナル / EP受容体 / 椎間板細胞 / NF-κβ / ﾌﾟﾛｽﾀﾉｲﾄﾞ / Ｗｎｔｼｸﾞﾅﾙ / ＥＰ受容体 |
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| Outline of Final Research Achievements |
Although the mechanism of intervertebral disc degeneration by inflammatory cytokines has been reported so far, the results showed that pathway mediated by TNF-α-PGE2 / EP receptor activates Wnt signal and induces intervertebral disc cell differentiation . These signals are important transcription signals involved in induction of inflammation and it was considered possible to act as a molecular switch of Wnt signal in intervertebral disc cells. In the future, if activation of Wnt signal by TNFα-PGE 2 signal could be suppressed at the receptor site, it could be possible to lead to a new molecular targeted therapeutic agent in disc degeneration.
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Report
(4 results)
Research Products
(4 results)
