| Project/Area Number |
20890061
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| Research Category |
Grant-in-Aid for Young Scientists (Start-up)
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| Allocation Type | Single-year Grants |
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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 Tokyo Medical and Dental University, 難治疾患研究所, 特任助教 (00466898)
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| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥3,302,000 (Direct Cost: ¥2,540,000、Indirect Cost: ¥762,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,742,000 (Direct Cost: ¥1,340,000、Indirect Cost: ¥402,000)
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| Keywords | 心房細動 / 心房リモデリング / 細胞外ATP / オートクライン作用 / マクロファージ / パラクライン作用 |
|---|
| Research Abstract |
Atrial dilatation is well-known contributor for atrial fibrillation, but its mechanism remains unclear. The aim of this study was to clarify the mechanism of atrial inflammation in stretched atrium. We found that mechanical stretch of atrial myocytes enhanced migration of macrophages. Further examinations revealed that atrial myocyte released ATP into the extracellular space, resulting in increased expression of chemokine by autocrine fashion. This mechanism may link between atrial dilatation and macrophage infiltration.
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