| Project/Area Number |
17K10851
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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 |
Neurosurgery
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| Research Institution | Meiji Pharmaceutical University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2022-03-31
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| Project Status |
Completed (Fiscal Year 2021)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2018: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2017: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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| Keywords | 脳梗塞 / アクアポリン / AQP11 / 総頚動脈結紮脳梗塞モデルマウス / AQP4 / 脳梗塞モデルマウス / 総頸動脈結紮 / 中大脳動脈梗塞 / 中大脳動脈脳梗塞 / 脳浮腫 / 疾患モデル動物 / 脳血管障害学 / 脳血管内外科学 |
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| Outline of Final Research Achievements |
The purpose of our study is to clarify the relation between brain infarction and AQP11.We generated brain infarction model mice which was ligated common carotid artery. Comparative analysis was performed for ligation time and reperfusion time. We investigated AQP11 expression for these models. AQP11 was increased that the combination model which was ligated for 15min and sacrificed after 30min. But, when it was sacrificed after 1 day later, AQP11 was decreased 20%. In the model which was ligated 1hr, AQP11 was decreased regardless of reperfusion time. This model was showed that AQP4 was increased as AQP11 was decreased. The expression of the microglia, astroglia and lysosomal-associated membrane marker gene were increased. Furthermore, our study was investigated the AQP11 expression of blood vessel endothelium model. We clarified that AQP11 was increased under hypertonic condition. For these results, it was suggested that AQP11 was participated in the transient cerebral ischemia.
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| Academic Significance and Societal Importance of the Research Achievements |
これまで脳梗塞とAQP11の関与は不明であったが、今回の研究から脳梗塞モデルマウスでは、脳梗塞の症状が明確に現れる成体のみならず、幼若マウスでもAQP11は同様に発現が変化することを判明した。梗塞時間の長さにより再還流後のAQP11の発現が増加することを示すことができたが、これは梗塞時間と再還流時間の組み合わせの１例である。さらにAQP11の発現が減少した今回のモデルでは常にAQP4、ミクログリア、アストログリア、リソソーム膜のマーカーが増加していたことより、これらのマーカーがの増減とAQP11の発現を制御することで脳梗塞の治療から予後の予測、延命への対応に寄与するものと考えられる。
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