MicroRNA overexpression to establish a new arrhythmia model for studying its molecular mechanism.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08179
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: The University of Tokushima (2016-2017); Oita University (2015)
• Principal Investigator: MORISHIMA Masaki 徳島大学, 病院, 特任講師 (40437934)
• Co-Investigator(Kenkyū-buntansha): 小野 克重 大分大学, 医学部, 教授 (40253778)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: microRNA / 心房細動 / 遺伝子改変動物 / 細胞内カルシウム

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.

Free Research Field

生理学、循環器病学、分子生物学