2013 Fiscal Year Final Research Report
The vessel repair mechanism in aortic aneurysm, focusing on the vascular smooth muscle.
Project/Area Number |
24791398
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
General surgery
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Research Institution | Kurume University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Keywords | 血管外科学 / 大動脈瘤 / 分子生物学 |
Research Abstract |
In this project, we found that activation of IL-6 signal(STAT3)are involved in the pathogenesis of murine and human aortic aneurysm, and also that in mice, STAT3 activation in smooth muscle cells are associated with apoptosis and proliferation. However, the IL-6 signal in smooth muscle cells did not affect the formation of experimental aortic aneurysm, and revealed that it is not critical to the aneurysm pathology. On the other hand, in the aortic dissection, knocking out smooth muscle's STAT3 showed greater susceptibility upon the BAPN and angiotensin infusion compared to wild type mice. Thus, we found a new insights, suggests that smooth muscle's STAT3 may play an important role in aortic dissection pathology.
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[Journal Article] Tenascin C protects aorta from acute dissection in mice2014
Author(s)
Kimura T, Shiraishi K, Furusho A, Ito S, sHirakata S, Nishida N, Yoshimura K, Imanaka-Yoshida K, Yoshida T, Ikeda Y, Miyamoto T, Ueno T, Hamano K, Hiroe M, Aonuma K, Matsuzaki M, Imaizumi T, Aoki H.
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Journal Title
Scientific Reports
Volume: 4
Pages: 4051
DOI
Peer Reviewed
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