Analysis of a novel mitochondrial protein AMF in energy metabolism

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860599
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Osaka University
• Principal Investigator: KATO Hisakazu 大阪大学, 医学(系)研究科(研究院), 特任研究員 (30589312)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: ミトコンドリア / ATP / 虚血

Outline of Final Research Achievements

Heart tissue consumes more energy than other organs to maintain cardiac pump function. Imbalances between energy demand and supply in an ischemic myocardium fall into the mechanical failure of heart. However, the mechanism by which mitochondrial ATP production is regulated under hypoxia is not fully understood. In this study, we revealed how a novel hypoxia-induced protein AMF affects mitochondrial ATP production under ischemic condition, mainly from the following experiments. (1) Immunoaffinity purification and mass spectrometric analysis revealed that AMF interacted with FoF1-ATP synthase complex. (2) Assessment of mitochondrial ATP concentration using FRET-based ATP biosensor allowed us to show that overexpression of AMF inhibited the decreases in mitochondrial ATP concentration under hypoxic condition in cultured cardiomyocytes and also in zebrafish heart. These results suggest that AMF functions as a guardian of ischemic heart via activating FoF1-ATP synthase.

Free Research Field

循環器内科学