2016 Fiscal Year Final Research Report
TGFb signaling pathways involved in rupture of aortic aneurysms
| 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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| Keywords | 大動脈瘤 / TGFβ / メカニカルストレス |
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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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| Free Research Field |
血管生物学
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