Molecular mechanisms of ischemic tolerance in the brain
| Project/Area Number |
24592314
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Osaka Prefecture University |
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Principal Investigator |
TAKAYUKI Nakajima 大阪府立大学, 生命環境科学研究科(系), 准教授 (30333644)
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| Co-Investigator(Kenkyū-buntansha) |
TAKENAKA Shigeo 大阪府立大学, 生命環境科学研究科, 准教授 (10280067)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 脳神経疾患 / 脳虚血 / 海馬 / 虚血耐性 / プロテオーム / ラット / プロテオーム解析 |
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| Outline of Final Research Achievements |
Neurons are vulnerable to ischemia, while they become tolerant to ischemia following exposure to a brief non-lethal period of ischemia known as ischemic preconditioning. This phenomenon is known as ischemic tolerance. We previously have reported that 3 min of ischemic preconditioning reduced 5 min ischemia-induced neuronal cell death in the hippocampal CA1 region. The aim of this study is to examine the altered expression of proteins in the CA1 region subjected to 3 min ischemic preconditioning using proteomic analysis. Proteomic analysis revealed that aconitase2, tubulin alpha 1A, protein-L-isoaspartate O-methiltransferase and voltage-dependent anion channel 1 were down-regulated in the CA1 region subjected to 3 min ischemic-preconditioning. The functional significance of the down-regulation of these proteins after 3 min ischemic preconditioning remains to be further studied.
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Report
(4 results)
Research Products
(5 results)
