Identification of target ion channels in various model of atrial fibrillation
| Project/Area Number |
15590784
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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 | The Cardiovascular Institute |
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Principal Investigator |
YAMASHITA Takeshi The Cardiovascular Institute, 第三研究部, 部長 (20302721)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 2004: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 2003: ¥200,000 (Direct Cost: ¥200,000)
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| Keywords | atrial fibrillation / ion channel / circadian rhythm / stress / pulmonary vein |
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| Research Abstract |
1)Spontaneous hypertensive rat
After recognizing that atrial fibrillation was easily induced in SHR rats, we have found that not ion channels but tissue fibrosis played a major role in the arrhythmogensis. In this model, the gene expression of inward and outward ion channels were preserved similarly to the control WKY rats.
2)Ion channels in the pulmonary veins
We have screened the gene expression of various ion channels and identified that one of pacemaker channels, HCN4, was abundantly expressed. In addition, the cardiomyocytes expressing HCN4 were compartmentalized along with aging, possibly leading to abnormal automaticity.
3)Stress-induced atrial fibrillation
We have created a new AF model induced by steroid hormone, where Kv1.5 was remarkably upregulated. Kv1.5 gene expression induced by steroid lead to progressive shortening of refractory period that underlies the arrhythmogenesis.
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Report
(3 results)
Research Products
(19 results)
