| Project/Area Number |
23590109
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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 |
Biological pharmacy
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| Research Institution | Tokyo University of Science (2013)
Kumamoto University (2011-2012) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HISATSUNE Akinori 熊本大学, 大学院先導機構, 特任准教授 (50347001)
KATSUKI Hiroshi 熊本大学, 大学院生命科学研究部, 教授 (40240733)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アクアポリン / 炎症 / サイトカイン / 桂皮 |
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| Research Abstract |
Aquaporin-5 (AQP5) is expressed in bronchial serous cells and exocrine gland, plays an important role for water homeostasis in airway. In the present study, we have examined the role of AQP5 for inflammatory response. Overexpression of AQP5 to various cells increased cytokine expression, steady level of phosphorylated ERK, and activity of NF-kappaB. Therefore, we assume that ERK and NF-kappaB are important for this new function of AQP5. Further, both AQP1 and AQP5-1CT chimera, which is converted C-terminal of AQP5 to AQP1, failed to increase cytokine expression, suggesting C-terminal of AQP5 is important for increased inflammatory response. Finally, we found extract of cinnamon as an inhibitor of ERK phosphorylation and cytokine expression by AQP5. Take together, we propose a new function of AQP5, as a cytokine signal enhancer, and cinnamon may be useful to control inflammatory response in AQP5 expressing cells.
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