| Project/Area Number |
20590577
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Kochi University |
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Principal Investigator |
KUMON Yoshitaka Kochi University, 教育研究部・医療学系, 准教授 (40215033)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIURA Tetsuro 高知大学, 教育研究部・医療学系, 教授 (50171145)
TAKEUCHI Hiroaki 高知大学, 教育研究部・医療学系, 講師 (90346560)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 酸化ストレス / 不安定プラーク / fPRL1 / 糖尿病 / 急性冠症候群 |
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| Research Abstract |
The mechanisms of rupture of plaque in acute coronary syndrome remains unclear, we histopathologically investigated the possible role of neutrophils resided in atheromatous plaque in the plaque rupture. The fPRL1 intensity of neutrophil cytoplasm was histologically high when neutrophils were in capillary vessels of the plaque originating from tunica adventitia. As soon as the activated neutrophils were extravasated into the plaque, however, the fPRL1 intensity of neutrophil cytoplasm significantly decreased, followed by exocytosis of fPRL1 on neutrophil surface. These neutrophils were alive and active in NADPH oxidase activity, followed by generation of reactive oxygen species (ROS), possibly resulting in plaque vulnerability which may cause the rupture of the vasculature.
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