Study on regulation mechanisms of cardiac rhythm and energy metabolism via mitochondria-sarcoplasmic reticulum coupling

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04674
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: General physiology
• Research Institution: University of Fukui
• Principal Investigator: Matsuoka Satoshi 福井大学, 学術研究院医学系部門, 教授 (00263096)
• Co-Investigator(Kenkyū-buntansha): 竹内 綾子 福井大学, 学術研究院医学系部門, 准教授 (00378704)
• Co-Investigator(Renkei-kenkyūsha): HIKIDA Masaki 秋田大学, 大学院理工学研究科, 教授 (60228715) ; SHIMAYOSHI Takao 九州大学, 情報基盤研究開発センター, 准教授 (60373510)
• Research Collaborator: IINO Satoshi 福井大学, 学術研究院医学系部門, 教授 (40242854) ; HORIGUCHI Kazuhide 福井大学, 学術研究院医学系部門, 准教授 (20377451) ; FUKAZAWA Yugo 福井大学, 学術研究院医学系部門, 教授 (60343745)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: ミトコンドリア / カルシウム / 心臓 / 数理モデル

Outline of Final Research Achievements

NCLX-knockout mice were created using the CRISPR-Cas9 method. Some of the homo-knockout mice show phenotypes different form wild type mice, such as low body weight, and abnormalities of heart and kidney. The Langendorff perfusion of mouse heart with a NCLX blocker (CGP-37157) tended to have decreased heart rate. In isolated mouse ventricular myocytes, CGP-37157 prolonged the 30 and 50% duration of action potential, and augmented the amplitude of Ca2+ transient probably due to the increase of SR Ca2+ content. A new comprehensive mathematical model of cardiac mitochondria was developed and published. A new mathematical model of sinoatrial cell, which contains the Ca2+ interaction between mitochondria and SR, was developed.

Free Research Field

生理学