| Project/Area Number |
26462745
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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 |
Emergency medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
柴藤 淳子 星薬科大学, 先端生命科学研究所, 客員助教 (10611121)
塩田 清二 星薬科大学, 先端生命科学研究所, 特任教授 (80102375)
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| Research Collaborator |
HORI Motohide
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | PACAP / pacap / brain / ischemia / DNA microarray / Proteomics / マイクロアレイ / 脳梗塞 |
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| Outline of Final Research Achievements |
Site-specific omics analysis of ischemic core (IC) and ischemic penumbra (IP) was performed by administering PACAP to a mouse cerebral infarction model. As a result, activation of blood clotting signal was confirmed in IP, and thrombolytic signal activation in IC was confirmed. Furthermore, suppression of excessive release of neuroendocrine hormone by IP administration of PACAP and IP prevented progression of secondary brain injury.
Furthermore, it was revealed that dephosphorylation of CRMP2 which had been confirmed to be altered by PACAP was strongly promoted especially at IP of 6 hours after administration of PACAP. Since it is known that CRMP2 changes to active form by dephosphorylation and controls axon formation and axon elongation action, the dephosphorylation action of CRMP2 by PACAP is important in the molecular mechanism of early neuroprotective action of cerebral infarction was suggested.
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