| Project/Area Number |
15KK0313
|
|---|
| Research Category |
Fund for the Promotion of Joint International Research (Fostering Joint International Research)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | The University of Tokushima (2016-2018)
Oita University (2015) |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
Singh Harpreet Drexel University, College of Medicine, Department of Pharmacology and Physiology, Associate professor
|
|---|
| Project Period (FY) |
2016 – 2018
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥11,960,000 (Direct Cost: ¥9,200,000、Indirect Cost: ¥2,760,000)
|
|---|
| Keywords | microRNA / 心房細動 / イオンチャネル / ミトコンドリア / 遺伝子改変ラット / ミトコンドリア障害 / 不整脈 / microRNA-30d / 心筋障害 |
|---|
| Outline of Final Research Achievements |
Our previous study has shown that microRNA-30d(miR-30d) is up-regulated in cardiomyocytes with persistent atrial fibrillation (AF), in response to cellular Ca2+-overload. However, mechanisms for miR-30d up-regulation in AF cardiomyocytes have not been elucidated. In this study, we investigated the mechanism how microRNA-30d (miR-30d) involved in the development of AF pathogenesis, we established a novel cardio-specific miR-30d overexpressed rat. MiR-30d overexpressed rats showed more vulnerable and short life span compared with wild type rats. The correlation of miR-30d expression between plasma and atrium was positively indicated in those rats. These data proposed circulating miRNA-30d as promise biomarkers and therapeutic targets in AF.
|
| Academic Significance and Societal Importance of the Research Achievements |
これまでに、持続性AFの病態を的確に現わすモデル動物が存在しなかったため、新規の不整脈治療薬開発のための基盤研究の妨げとなってきたが、我々が樹立した心筋特異的miR-30d過剰発現ラットを用いて生理学的解析を行うことで、AFの病因に関わる新たな因子の同定につながることが期待される。さらに、本研究で着目したmiR-30dがAFの病態を良好に反映するバイオマーカーとして、今後臨床応用できる可能性がある。
|
