2015 Fiscal Year Final Research Report
The role of mitochondrial protein MENT in myocardial ischemic preconditioning
Project/Area Number |
26860559
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Cardiovascular medicine
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Research Institution | Osaka University |
Principal Investigator |
Kioka Hidetaka 大阪大学, 医学(系)研究科(研究院), 寄附講座助教 (70642099)
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Project Period (FY) |
2014-04-01 – 2016-03-31
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Keywords | 心筋虚血 / ミトコンドリア / エネルギー代謝 |
Outline of Final Research Achievements |
Most eukaryotic cells generate ATP through oxidative phosphorylation system (OXPHOS) to support cellular activities. We have recently established the method for the selective measurement of intra-mitochondrial ATP levels and have identified the hypoxia-inducible protein MENT as a positive regulator of OXPHOS by cultured cell-based experiments. In this study, we introduced a FRET-based ATP biosensor named ATeam into zebrafish heart and examined in vivo role of MENT under hypoxia. We established the in vivo ATP imaging technique. This technique clearly revealed that MENT-expressing cardiomyocyte populations showed preserved contractility with increased intra-mitochondrial ATP concentration in hypoxic condition. Futhermore, we showed that MENT expression is enhanced in the risk area in canine ischemic preconditioning model. These results suggest that MENT functions as a guardian of hypoxic tissue and could become a therapeutic target for hypoxia-related diseases.
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Free Research Field |
循環器病学
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