The mechanisms underlying the enlargement of intracranial aneurysm focused on hemodynamic stress loading
| Project/Area Number |
26861145
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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 |
Neurosurgery
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| Research Institution | Kyoto University |
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Principal Investigator |
TOMOHIRO AOKI 京都大学, 医学(系)研究科(研究院), 准教授 (40633144)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 脳動脈瘤 / 血流 / 内皮細胞 / マクロファージ / MCP-1 / 乱流 / ずり応力 / 炎症 / 低ずり応力 / 細胞分裂 / 遊走因子 |
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| Outline of Final Research Achievements |
Intracranial aneurysm (IA) is a socially important disease as a major cause of subarachnoid hemorrhage. We have, recently, clarified contribution of MCP-1-mediated macrophage infiltration and macrophage-evoked inflammatory responses to the pathogenesis of IA. In the other point of view, hemodynamic status surrounding IA lesion is dramatically changed during IA progression, high wall shear stress in formation and low walls shear stress with concomitant turbulent flow in progression. Based on these findings, we have analyzed the causative relationship between hemodynamic stress and MCP-1 expression in these cells of IA walls. We found that both high wall and low shear stress with concomitant turbulent flow induced MCP-1 expression in culture endothelial cells and that, in rat model of IAs, MCP-1 expression was sustained once after induced at the early stage. These results suggest that, independence of dramatically changes in hemodynamic status, MCP-1 expression is sustained.
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Report
(3 results)
Research Products
(5 results)
