| Project/Area Number |
25861236
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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) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 大動脈解離 / ピオグリタゾン / 塩分過剰 / IL-17 |
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| Outline of Final Research Achievements |
In this project, we investigated whether pioglitazone suppresses aortic dissection. Unexpectedly, pioglitazone worsened the aortic dissection in mice. We hypothesized that sodium retention by pioglitazone might be the underlying mechanism. In fact, excessive sodium intake worsened aortic dissection through IL-17 pathway. Transcriptome analysis of aortae before the onset of aortic dissection showed strong induction of proinflammatory genes and suppression of extracellular matrix genes. Deletion of IL-17 gene resulted in the augmented expression of extracellular matrix genes and enhanced collagen deposition. From these results, we concluded that IL-17 suppresses the extracellular matrix synthesis, which in turn worsens aortic dissection. We will continue to explore the mechanism of aortic dissection, focussing on the roles of IL-17 and extracellular matrix.
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