| Project/Area Number |
11671524
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Tokyo Medical University |
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Principal Investigator |
MIURA Hitoshi (2000) Tokyo Medical University Medicine Lecturer, 医学部, 講師 (50246302)
本間 豊彦 (1999) 東京医科大学, 医学部, 講師 (60229268)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBASAKI Futoshi Tokyo Merropolitan Institute of Medical Science Department of Moleculae Physiology Director, その他・研究員 (90300954)
WATABANE Yasuo Tokyo Medical University, Medicine, Associate Professor, 医学部, 助教授 (70183720)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Brain ischemia / ischemic neuronal death / mitochondrial dysfunction / calcineurin / immunosuppressant / Cyclosporin A / 神経細胞死 / 脱リン酸化酵素 / MRI / 三次元構築 / MPT |
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| Research Abstract |
Brain ischemia leads to severe damage in the form of delayed neuronal cell death. We have been investigated the mechanisms of delayed neuronal cell death in terms of the mechanisms of immunosuppressant, such as cyclosporin A (CsA) and FK506. We show here the drastic neuroprotection of the CsA in the forebrain ischemia is not only due to inhibition of calcineurininduced cell death through dephosphorylation of proapoptotic protein Bad, but also due to protection of mitochonorial damage which is caused by the MPT (Mitochondrial Permeability Transition) pore formation through cyclophilin D (CyPD), one of the prolyl cis/trans isomerase family members.
These results shed light on the clinical application and development of new drugs for the treatment of ischemic damage in the brain as well as in the heart and liver.
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