| Project/Area Number |
22791264
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
General 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) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 血管外科学 / 大動脈瘤 / サイトカイン / 大動脈解離 / 血管 / 分子生物学 |
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| Research Abstract |
In this project, we investigated the hypothesis that IL-6/JAK/STAT pathway is activated and involved in the pathogenesis of abdominal aortic aneurysm(AAA), using human AAA tissue culture and mouse model of AAA. We found that human AAA tissue secrets large amount of IL-6 in culture media, and JAK/STAT pathway is involved in the secretion of a subset of inflammatory cytokines. We also found that JAK/STAT pathway is activated in mouse model of AAA during the rapid expansion of the diameter. However, macrophage-specific deletion of SOCS3 gene(mSOCS3-KO), which should enhance the IL-6 signal, did not affect the formation of AAA in mice. Unexpectedly, mSOCS3-KO showed greater susceptibility to acute aortic dissection(AAD) upon the angiotensin II infusion compared to wild type mice. Thus, macrophage IL-6 signal appears to be dispensable for AAA development, but essential to AAD development in mouse models.
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