| Project/Area Number |
25670622
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neurosurgery
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| Research Institution | University of Yamanashi |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
KINOUCHI Hiroyuki 山梨大学, 総合研究部, 教授 (30241623)
SHINOZAKI Youichi 山梨大学, 総合研究部, 講師 (10443772)
SHIGETOMI Eiji 山梨大学, 総合研究部, 助教 (00631061)
SHIBATA Keisuke 山梨大学, 総合研究部, 助教 (50580411)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | グリア細胞 / アストロサイト / 脳卒中 / 虚血耐性 / グリア伝達 / グリア / P2受容体 / 虚血 / P2X7受容体 |
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| Outline of Final Research Achievements |
Using a preceding sub-lethal ischemic insult, preconditioning (PC), is an attractive strategy for protecting neurons by inducing ischemic tolerance in the brain. Although the underlying molecular mechanisms have been studied extensively, almost all experiments have been performed on neurons. Here, using a middle cerebral artery occlusion model in mice, we show that astrocytes have an essential role in the induction of ischemic tolerance. PC caused activation of astrocytes, which was essential for the induction of ischemic tolerance. As for the mechanisms, we found that P2X7 receptors were dramatically upregulated in activated astrocytes, which was essential for the ischemic tolerance. Unlike previous reports focusing on neuron-based mechanisms, our results show that astrocytes play indispensable roles in inducing ischemic tolerance.
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