2017 Fiscal Year Final Research Report
Molecular mechanism of worsening aortic dissection by high salt via IL-17 pathway
| Project/Area Number |
16K19973
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular surgery
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| Research Institution | Kurume University |
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Principal Investigator |
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Keywords | 大動脈解離 / 塩分過剰 / IL-17 / 細胞外マトリックス |
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| Outline of Final Research Achievements |
In this project, we investigated the mechanism of worsening aortic dissection by high salt intake and the involvement of IL-17. High salt induced IL-17 receptor expression without affecting plasma IL-17, and activated NFkB in aorta in an IL-17-dependent manner, suggesting the increase the sensitivity of aortic tissue to IL-17. In addition, deletion of IL-17 gene showed higher activity of Smad2, upregulation of ECM genes, and increase in medial collagen fibers in aorta. Interestingly, high salt induced expression of Smad7, a negative regulator of Smad signaling, and suppressed Smad2 activation in an IL-17-dependent manner. We propose that high salt and IL-17 synergistically dysregulate ECM metabolism in aorta to exacerbate AD.
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| Free Research Field |
血管外科、分子血管病態学
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