| Project/Area Number |
16K19016
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | University of Yamanashi |
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Principal Investigator |
HIRAYAMA Yuri 山梨大学, 医学部附属病院, 薬剤師 (30732804)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | グリア細胞 / アストロサイト / 脳梗塞 / 虚血耐性 / ATP受容体 / 脳虚血耐性 / P2X7受容体 / HIF-1α / Preconditioning / 脳・神経 |
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| Outline of Final Research Achievements |
Brain ischemic tolerance is an endogenous neuroprotective mechanism, whereby an experience of mild ischemic episode (preconditioning; PC) produces resilience to subsequent much severe ischemic injury. We previously showed that PC-induced activation of astrocytes, and their subsequent expression of HIF-1α is responsible for ischemic tolerance. Although PC also increased HIF-1α in neurons, this was not involved in ischemic tolerance. Here, we show the difference in mechanism of HIF-1α increase between neurons and astrocytes, and answer why astrocytic HIF-1α is more important.
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