| Project/Area Number |
17K08610
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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 |
General pharmacology
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| Research Institution | Fukuoka University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
田頭 秀章 福岡大学, 医学部, 講師 (90735028)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | イオン輸送体 / 心不全 / 心肥大 / 病態モデル動物 / 創薬 |
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| Outline of Final Research Achievements |
Solute carrier (SLC) transporters are membrane proteins that facilitate the transport of substrates across biological membranes. We confirmed that the targeted SLC transporter can transport Ca2+, using mammalian cell expression system. Interestingly, cardiac-specific transgenic mice of the target SLC transporter exhibited cardiac hypertrophy, reduced cardiac function, and early sudden death. Furthermore, we observed abnormal Ca2+ transients in cultured cardiac myocytes from the cardiac-specific transgenic mice. These results suggest that upregulation of the targeted SLC transporter may induce cardiac hypertrophy/heart failure. We established the screening system for the specific inhibitors, which might be useful therapeutically.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究では、SLCトランスポーター群の中から新規なCa2+輸送体（標的SLC輸送体分子）を見出した。この遺伝子改変マウスを用いた病態生理学的解析から、標的SLC輸送体分子は、心肥大・心不全の誘発因子である可能性が示唆された。本研究成果は、心肥大・心不全の病態解明に貢献するのみならず、新たな心不全治療薬の開発に繋がることが期待される。
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