| Project/Area Number |
26450295
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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 |
Aquatic life science
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
HIROI Junya 聖マリアンナ医科大学, 医学部, 准教授 (20350598)
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| Research Collaborator |
MARUYAMA Kouichi 独立行政法人放射線医学総合研究所, 福島再生支援本部, 主任研究員 (70349033)
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| Project Period (FY) |
2014-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 塩類細胞 / トランスポーター / Na+/H+交換体 / Rh因子 / デコンボリューション / 超解像イメージング / メタボロン |
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| Outline of Final Research Achievements |
Localization patterns of NHE3b and Rhcg1 in rainbow trout ionocytes were examined with newly-raised antibodies. The immunoreactivity of NHE3b and Rhcg1 looked likely to be colocalized at the apical membrane of the ionocytes, but the higher-resolution imaging revealed that NHE3b was diffused and located rather subapically in freshwater-acclimated trout, whereas that NHE3b was concentrated at the apical membrane, being more colocalized with Rhcg1, following transfer to deionized water or acidic water. These morphological changes would imply that ammonia-dependent sodium uptake by the Rh-NHE metabolon is more active in low-sodium and low-pH environments.
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| Academic Significance and Societal Importance of the Research Achievements |
塩類細胞の既知の機能であるNa+の取り込みに加え，本研究では新たにH+とアンモニアの排出に注目し，これらの3機能が連携していることと外部環境変化に応じて連携が亢進されることを明らかにすることができたが，H+の排出は体液の酸塩基調節のかなめであり，アンモニアの排出は窒素代謝の最終過程であるため，これらの成果は魚類生理学・水産増養殖学の両面から重要である．また，塩類細胞のサブタイプによるK+の排出機構を明らかにしたが，Cs+はK+と同じ挙動を示すため，この成果は放射性Csによる魚類の汚染と除染のメカニズムを明らかにするうえで重要である．
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