Ctarification of pathophysiology of remodeling after intracranial artery inJury model in mice in dystipidemia
| Project/Area Number |
22791341
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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 |
Cerebral neurosurgery
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| Research Institution | Osaka University |
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Principal Investigator |
MUNEHISA Shimamura 大阪大学, 連合小児発達学研究科, 寄附講座准教授 (60422317)
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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 |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 脳血管内外科学 / リモデリング / 脳血管形成術 / 脂質異常症 / マウス / 頭蓋内脳動脈 / 血管障害モデル / 血管リモデリング / 血管傷害モデル |
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| Research Abstract |
In the present study, we established the intracranial artery injury model in mice. The temporal profile of remodeling was as follows : neointimal formation was grown from 28 days after injury ; re-endothelialization was started from day 7 ; inflammatory cells were observed from day 7 in the adventitia. These processes of remodeling were quite different from those in extracranial arteries. Using this model, we examined whether dyslipidemia had influences on the process of remodeling. To demonstrate it, Lp(a) transgenic mice, which showed high serum Lp(a) level, were exposed to the injury model. Unexpectedly, the extent of neointimal formation and the rate of re-endothelialization were not different between the groups. From the viewpoints, Lp(a) level might have no influences on remodeling after the injury in intracranial arteries.
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Report
(3 results)
Research Products
(2 results)
