Study on ion channel remodeling in atrial fibrillation
| Project/Area Number |
13670775
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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) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | atrial fibrillation / ion channel / gene expression / remodeling / 不整脈 / Kv1.5 / 概日リズム / アルコール |
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| Research Abstract |
To investigate the molecular mechanisms underlying the initiation and maintenance of atrial fibrillation, we analyzed the gene expression of ion channels expressed in the rat atrium including Na^+ channel, Ca^<2+> channel, voltage-dependent K^+ channels, inwardly-rectifying K^+channels, and HCN channels. Various factors known to cause feasibility of atrial fibrillation induction modified the ion channel expression in various ways. Rapid atrial pacing caused immediate upregulation of Kv1.5 and simultaneous downregulation of Kv4.2, Kv4.3, HCN4, and auxiliary subunit of L-type Ca2^+ channel. The gene expression of Kv1.5 and Kv4.2 showed a characteristic circadian variation reverse to each other. Cortisol induced upregulation of Kv1.5 and Kir 2.2. Alcohol caused a different type of ion channel remodeling: upregulation of Kv1.5 and HCN4. These results indicated that various factors surrounding atrial fibrillation caused various types of ion channel remodeling, necessitating the concept of targeting the channel according to the characteristics of the patients.
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Report
(3 results)
Research Products
(21 results)
