Novel apoptosis-inducing ligand ORAIP plays a critical role in cerebral ischemia/reperfusion injury
| Project/Area Number |
16K20021
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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 |
Neurosurgery
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| Research Institution | Yokohama City University |
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Principal Investigator |
TAKASE Hajime 横浜市立大学, 医学研究科, 共同研究員 (00549975)
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| Research Collaborator |
SUENAGA Jun
KISHIMOTO Masao
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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: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 酸化ストレス / アポトーシス / 脳虚血 / 再灌流障害 / ORAIP / apoptosis / oxidative stress / cerebral ischemia / repercussion injury / 脳血管障害学 / 脳保護療法 / 脳梗塞 / 虚血再灌流 / eIF5A |
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| Outline of Final Research Achievements |
Oxidative stress plays a critical role in the pathogenesis of ischemia/reperfusion (I/R) injury that leads to apoptosis. We previously identified a novel apoptosis inducing humoral factor in a conditioned medium of cardiac myocytes subjected to hypoxia/reoxygenation (H/R). We named this novel post-translationally modified secreted form of eIF5A as Oxidative stress-Responsive Apoptosis Inducing Protein (ORAIP). We confirmed that rat myocardial I/R injury was significantly suppressed by treatment with neutralizing anti-ORAIP monoclonal antibodies (mAbs). The purpose of this study is to investigate whether the same mechanism is involved in cerebral I/R injury. We found the expression of ORAIP in various types of neural cells in the ischemic penumbra region after cerebral I/R. Anti-ORAIP mAb-treatment also significantly decreased the cerebral infarct volume compared with vehicle-treatment group.
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Report
(3 results)
Research Products
(5 results)
