| Project/Area Number |
15K20898
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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 |
Pathological medical chemistry
Cardiovascular medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Research Collaborator |
Yanagisawa Hiromi 筑波大学, 生命領域学際研究センター, 教授 (40746301)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 大動脈瘤 / TGFβ / メカニカルストレス / 大動脈瘤破裂 / TGF-β / 血管平滑筋細胞 / 細胞外マトリックス |
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| Outline of Final Research Achievements |
In the Fbln4SMKO (mice model for ascending aortic aneurysm; SMKO) mice, treatment with TGF-β neutralizing antibody (1D11) leads to aneurysm rupture. We examined conditions for 1D11 treatment and signaling pathways involved in aneurysm rupture in SMKO mice. First, We considered concentration, administration period for 1D11 treatment and finally established suitable conditions for 1D11 treatment leadding rupture. In addition, we found that the expression of ACE (angiotensin converting enzyme), Egr1 (Early growth response-1) and Thrombospondin-1 increased in ascending aorta after TAC procedure, which enhanced mechanical stress in the aorta. Thus, we denied these molecules as mechanical stress response factor and hypothesized that mechanical stress response factor might involved in aneurysm initiation.
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