Deciphering molecular mechanisms underlying the unconventional extracellular mitochondria release
| Project/Area Number |
17F17413
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| Research Category |
Grant-in-Aid for JSPS Fellows
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| Allocation Type | Single-year Grants |
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| Section | 外国 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Osaka University |
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Principal Investigator |
望月 秀樹 大阪大学, 医学系研究科, 教授 (90230044)
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| Co-Investigator(Kenkyū-buntansha) |
CHOONG CHI JING 大阪大学, 医学(系)研究科(研究院), 外国人特別研究員
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| Project Period (FY) |
2017-11-10 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 2019: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2018: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2017: ¥600,000 (Direct Cost: ¥600,000)
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| Keywords | Mitochondria / Mitophagy / Parkin / Parkinson's disease / Rotenone / mitochondria / rotenone / parkin |
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| Outline of Annual Research Achievements |
Selective removal of damaged mitochondria by mitophagy is crucial for maintaining mitochondrial quality control and cell viability. Here we demonstrate an alternative quality control pathway mediated by extracellular mitochondria release. We performed real time tracking of fluorescence-labelled mitochondria in cultured cells and observed release of mitochondria into extracellular space. Using mitochondrial toxin treatment and parkin gene overexpression and knockdown approaches, we found that mitochondrial stress and perturbation of mitophagy induce greater extracellular mitochondria release. Remarkably, fibroblasts and CSF from Parkinson’s disease patients carrying parkin mutations showed increased extracellular mitochondria release compared to control subjects, providing evidence in clinical context that impairment of conventional mitophagy prompts the alternative pathway.
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| Research Progress Status |
令和元年度が最終年度であるため、記入しない。
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| Strategy for Future Research Activity |
令和元年度が最終年度であるため、記入しない。
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Report
(3 results)
Research Products
(5 results)
