| Project/Area Number |
14571467
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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 |
UCHINO Hiroyuki Tokyo Medical University, Medicine, Assistant Professor, 医学部, 講師 (60266476)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBASAKI Futoshi Tokyo Metropolitan Institute of Medical Science, Department of Molecular Physiology, Director, 東京都臨床医学総合研究所, 研究員
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Calcineurin / Cyclophillin D / CsA / CsJ / NCX / MPT / Brain ischemia / DNA chip / Knock out mouse / 脳虚血 / 神経細胞死 / Cyclophilin D / Calcineurin / MPT / CSJ / Ca2+ exchanger / 脳保護 |
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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 a cyclosporin A(CsA) and FK506. From our results, Calcineurin and immunophilin signal transduction casca* play an important roles for neuroprotection, Especially, mitochondrial isomerase cyclophillinD paly a pivotal role to regulate the MPT(Mitochondrial Permeability Transition)pore formation, one of the prolylcis/trans isomerase family members.
We also need further analysis to explore more mechanisms.
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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