| Project/Area Number |
12670598
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | FUKUI MEDICAL UNIVERSITY |
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Principal Investigator |
YONEDA Makoto FUKUI MED. UNIV., University Hospital, LECTURER, 医学部附属病院, 講師 (70270551)
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| Co-Investigator(Kenkyū-buntansha) |
KURIYAMA Masaru FUKUI MED. UNIV., Faculty of Medicine, PROFESSOR, 医学部, 教授 (80107870)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2002: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | MELAS / ANGIOPATHY / CYBRIDS / ミトコンドリア血管症 / ミトコンドリア遺伝子変異 / MELAS症候群 / ヒト脳血管内皮細胞 |
|---|
| Research Abstract |
Mitochondrial encephalplathy, myopathy, lactic acidosis and strokelike episodes (MELAS) syndrome is characterized by a mitochondrial DNA (mtDNA) mutation (A3243G) and mitochondrial angiopathy in the brain. To investigate the pathogenic mechanism for mitochondrial angiopathy, we tried to construct cybrids that carry the MELAS mutation and were derived from human brain vessel endothelial cells. First, we determined the optimal concentration of ethidium bromide (EtBr) to reduce or remove mtDNA from the blood vessel endothelial cells. We then introduced the platelet mitochondria from MELAS patients into the blood vessel endothelial cells lacking mtDNA. Cybrids carrying the mtDNA mutation were hard to survive. We should further investigate the optimal media condition to get cybrids survived.
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