| Project/Area Number |
22590804
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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 |
Circulatory organs internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SASANO Tetsuo 東京医科歯科大学, 大学院・保健衛生学研究科, 准教授 (00466898)
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| Research Collaborator |
FURUKAWA Tetsushi 東京医科歯科大学, 難治疾患研究所, 教授 (80251552)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 心房細動 / マクロファージ / 炎症 / ATP / ギャップジャンクションチャネル / 伸展刺激 / 線維化 / パラクライン作用 / メタボリック症候群 |
|---|
| Research Abstract |
Although atrial dilatation is well-known risk for atrial fibrillation, the mechanism linking them remains unclear. We aimed to elucidate the mechanism that mechanical stretch induced atrial inflammation, especially focusing the infiltration of macrophage. The stretched atrial myocytes released ATP in extracellular space, which evoked migration of macrophage. The gap junction family channel including pannexin-2 contributed this mechanism. Murine model of atrial stretch showed infiltration of macrophage, followed by inflammation, fibrosis, and atrial tachycardia. A gap junction channel blocker inhibited these changes. This mechanism may play pivotal role for atrial fibrillation under conditions with atrial dilatation.
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