| Project/Area Number |
15K08179
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | The University of Tokushima (2016-2017)
Oita University (2015) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小野 克重 大分大学, 医学部, 教授 (40253778)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | microRNA / 心房細動 / 遺伝子改変動物 / 細胞内カルシウム / 遺伝子改変ラット / ミトコンドリア障害 / microRNA-30d / Ａｎｇｉｏｔｅｎｓｉｎ ＩＩ / イオンチャネル / 疾患モデルラット |
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| Outline of Final Research Achievements |
We have previously shown that miR-30d is up-regulated in cardiomyocytes with persistent atrial fibrillation (AF), in response to cellular Ca2+-overload. It is well-known that abnormal Ca2+ dynamics may lead to the development of AF, however, mechanisms for microRNA-30d (miR-30d） up-regulation in AF cardiomyocytes have not been elucidated. To investigate whether Ca2+ overload regulates miR-30d expression in adult or neonatal rat cardiomyocytes, we infused angiotensin II (Ang II; 1.68 mg/kg/day) or noradrenaline (NA; 5.4 mg/kg/day) for 2 weeks via osmotic minipump into adult Wistar rats, because Ang II and NA are well-known drivers for onset of AF. Acute- or long-term stimulation of cardiomyocytes by Ang II induces elevation of miR-30d expression independently of the changes in blood pressure. The correlation of miR-30d expression between plasma and atrium was positively indicated. Our data would propose circulating miRNA-30d as promise biomarkers and therapeutic targets in AF.
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