| Project/Area Number |
15K15181
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied pharmacology
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| Research Institution | Kanazawa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
川井 恵一 金沢大学, 保健学系, 教授 (30204663)
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| Co-Investigator(Renkei-kenkyūsha) |
Nakamichi Noritaka 金沢大学, 薬学系, 准教授 (10401895)
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| Research Collaborator |
Nakamura Yoshinobu 金沢大学, 大学院
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | トランスポーター / プロスタグランジン / 炎症 / 発熱 / 抗炎症薬 / マクロファージ / 内毒素 / 免疫 / 開口分泌 / 大腸癌 |
|---|
| Outline of Final Research Achievements |
The present study indicates that an important chemical mediator prostaglandin (PG) E2 is transported into acidic organelles including lysosome via OATP2A1, which is a transporter with high affinity to PGE2, in macrophages activated under inflammatory condition, and then it is secreted by exocytosis. Since genetic and chemical suppression of Oatp2a1 attenuated endotoxin-induced fever in rodent models, OATP2A1 is expected to be a novel target for antipyretic drugs.
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