2016 Fiscal Year Final Research Report
Identification of molecular factors related to PACAP neuroprotective effect in ischemic brain
| 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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| Research Collaborator |
HORI Motohide
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | PACAP |
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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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| Free Research Field |
分子生物学
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