| Project/Area Number |
03670470
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | HYOGO COLLEGE OF MEDICINE |
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Principal Investigator |
MATSUYAMA Tomohiro HYOGO COLLEGE OF MEDICINE INTERNAL MEDICINE (V) ASSOCIATE PROFESSOR, 医学部, 講師 (10219529)
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| Co-Investigator(Kenkyū-buntansha) |
UYAMA Osamu HYOGO COLLEGE OF MEDICINE INTERNAL MEDICINE (V) ASSOCIATE PROFESSOR, 医学部, 助教授 (00185076)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Transient Ischemia / Copper-Zinc Superoxide Dismutase / Manganese Superoxide Dismutase / In Situ Hybridization Histochemistry / Immunocytochemistry / Delayed Neuronal Death / Ischemic Tolerance Phenomenon / Mongolian Gerbil / Copper-Zinc-Superoxide Dismutase / Manyanese-Superoxide Dismutase / Immunoryto chemistry / 虚血負荷応答 / Superoxide Dismutase / in situ hybridization histochemistry / 免疫組織化学 / 海馬 / 酸素ストレス |
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| Research Abstract |
To assess the role of copper, zinc- and manganese-superoxide dismutase (CuZnSOD and MnSOD) in regulating cellular antioxidant defense. we studied the induction of mRNAs encoding CuZnSOD or MnSOD by an in situ hybridization technique and of their proteins by an immunocytochemical method in the gerbil hippocampus following transient global ischemia. In sham-operated animals, the CA1 pyramidal neurons containing a large amount of CuZnSOD produced only a small amount of MnSOD. suggesting that the cellular vulnerability to ischemia is associated with the content of intracellular MnSOD. Transient ischemia for 5 min, which leads to delayed neuronal death in CA1, transiently stimulated both SOD mRNAs to increase without the production of SOD proteins. These results suggest that the reduction in the synthesis of endogenous SODs is important in the neurons which are vulnerable to ischemic insult. On the contrary, the ischemia for 2 min that induced the ischemic tolerance by CA1 pyramidal neurons, showed an increase in the expression of MnSOD mRNA in CA1 with a significant increase in MnSOD immunoreactivity. The same insult has less effects on the expression of CuZnSOD mRNA and its protein. These findings indicate the selective induction of MnSOD by the cells which acquired the ischemic tolerance, and suggest that the MnSOD has an important role in the acquisition of ischemic tolerance by vulnerable neurons, probably as an intracellular antioxidant enzyme.
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