| Project/Area Number |
15K19366
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
XU DongZhu 筑波大学, 医学医療系, 助教 (20616651)
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| Research Collaborator |
Chen Peng-Sheng Indiana university, Krannert institute of Cardiology, 教授
Chen Zhenhui Indiana university, Krannert institute of Cardiology, 准教授
Murakoshi Nobuyuki 筑波大学, 医学医療系循環器内科, 講師
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 心房細動 / 肥満 / Nampt / カルシウムハンドリング / atrial fibrillation / obesity / NADPH / Ca handling / 心臓電気生理 / Nampt/NAD+/Sirtuin系 / カルシウム調節 |
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| Outline of Final Research Achievements |
In electrophysiological study, Nampt+/-showed increased AF inducibility (80.0% in Nampt+/-+ND, 44.0% in Nampt+/++ND, p<0.05) and duration compared to Nampt+/+, and HFD accelerated longer duration than ND (15.21±5.75 in Nampt+/-+HFD, 8.83±3.33 in Nampt+/-+ND, 6.17±2.66 in Nampt+/++HFD, 3.39±1.07 in Nampt+/++ND, p<0.05). There was no significant difference in fibrotic area between all group. The gene and protein expression levels of Nampt in the atria were decreased by half in the Nampt+/-, and further decreased in Nampt+/-+HFD. The gene expression levels of calcium handling-related molecules Ryr2 and Atp2a2 were decreased in Nampt+/- compared to those of Nampt+/+. These findings suggested that genetic reduction of Nampt increased AF inducibility and duration partially through modulating calcium handling pathway without obvious structural alterations.
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