| Project/Area Number |
15H06006
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | イオンチャネル / 心筋細胞 / 心房細動 / クロライドチャネル / 不整脈 / 肺静脈 / Cl- チャネル |
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| Outline of Final Research Achievements |
Pulmonary vein (PV) are known to be the origin of atrial fibrillation (AF), the most frequent arrhythmia. We have observed the novel Cl- current in rat PV cardiomyocytes, and revealed that the current facilitates the arrhythmogenicity of PV. The purpose of the current study is to isolate cDNA of ion channel responsible for the Cl- current before we identify the actual whole molecule. Because the Cl- current of PV is hyperpolarization-activated, we tried to find splice variants of well-known hyperpolarization-activated Cl- channel, Clcn2, by RT-PCR. We could not find any variants from rat PV but Clcn2 itself. Immunostaining revealed Clcn2 expression on the plasma membrane of rat PV. Properties of the channel cloned from rat PV are exactly same as those of Clcn2 reported previously, different from the PV current. These results suggest that Clcn2 functionally expressed in rat PV, and regulated by unknown axillary proteins. We will unveil the axillary subunits by proteomics in the future.
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