| Project/Area Number |
13671603
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Nagoya City University |
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Principal Investigator |
TAKEUCHI Akinori Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (50254305)
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| Co-Investigator(Kenkyū-buntansha) |
ASAI Kiyofumi Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (70212462)
SOBUE Kazuya Nagoya City University, Graduate School of Medical Sciences, Research Associate, 大学院・医学研究科, 助手 (90264738)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Edema / Aquaporin / Astrocytes / Brain / Culture / Trauma |
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| Research Abstract |
Aquaporins, water channels, are a family of water-selective transporting proteins, that play an important role in water transport in the brain. Firstly, the expression of AQP family was investigated thoroughly in the central nervous system. In the brain, we detected the transcripts of AQP3, AQP4, AQP5, AQP8, AQP9 in astrocytes using the reverse transcription-PCR. These results suggest that AQP in astrocytes have roles in not only water transport but also other unknown functions. Secondly, regulatory mechanisms of AQP expressions were also investigated. The expression of AQP4 was down-regulated by protein kinase C (PKC). The expression of AQP5 was down-regulated by protein kinase A (PKA). The expression of AQP9 was up-regulated by PKA and down-regulated PKC. The p38 mitogen-activated proteinkinase (p38 MAPK) regulated the expression of AQP4 and AQP9. These results suggest that the expressions of AQPs are intricately regulated according to the conditions. Third, we examined the changes of AQP expressions under hypoxic stress. The expressions of AQP4 and AQP9 were up-regulated by hypoxia, but precise mechanisms for their regulation are still unclear. Further studies are needed to clarify the mechanisms.
New therapeutic method for brain edema may be developed from our basic data. The agent of regulation of AQP expression or AQP antibodies might be new medicines for brain edema.
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