| Project/Area Number |
24791478
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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 |
Thoracic surgery
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| Research Institution | Kurume University |
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Principal Investigator |
OHNO satoko 久留米大学, 医学部, 助教 (80569418)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 大動脈解離 / マクロファージ / 炎症応答 / サイトカイン / 分子生物 / 分子生物学 / 炎症 / 血管平滑筋 / 細胞分裂 / 血管 |
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| Outline of Final Research Achievements |
We tested the hypothesis that macrophage IL-6 signal is involved in the pathogenesis of aortic dissection (AD). We found that macrophage-specific SOCS3-KO (mSOCS3-KO), in which IL-6 signal is enhanced specifically in macrophages, developed distructive aortic dissection more frequently than wild type mice (WT) upon angiotensin II stimulation. Transcriptome analyses showed higher expression of cell cycle and inflammatory genes in mSOCS3-KO than in WT before the onset of AD. In mSOCS3-KO, macrophages were preferentially differentiated to proinflammatory M1, indicating enhancement of aortic inflammation. Human AD samples showed higher activation of macrophage IL-6 signal and cell cycle in adventitia and outer media close to the site of dissection than the remote aortic walls. These results indicate that excessive activation of IL-6 signaling in macrophages leads to the destructive inflammation in AD. We will investigate whether anti-inflammatory M2 can stabilize AD in the future.
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