Role of changes in the function of G-protein coupled receptors due to cholesterol depletion from the cell membrane in cardiovascular protection
| Project/Area Number |
15K08254
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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) |
朔 啓二郎 福岡大学, 医学部, 教授 (40183371)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 高血圧 / 脂質 / 循環器 / 循環器・高血圧 |
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| Outline of Final Research Achievements |
We determined whether changes in the function of angiotensin II type 1 (AT1) receptor receptor due to cholesterol depletion from cardiovascular cell membranes through statin treatment affects blood pressure. Angiotensin II-induced increase in mean blood pressure was significantly suppressed by pretreatment with rosuvastatin in mice. Angiotensin II-induced inositol phosphate production through AT1 receptor was suppressed by cholesterol depletion from cell membranes using rosuvastatin or methyl-beta-cyclodextrin. Angiotensin II-induced activation of AT1 receptor reduced after cholesterol depletion, and this may contribute to blood pressure reduction.
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| Academic Significance and Societal Importance of the Research Achievements |
心血管病は、死亡原因の第２位であり、その克服は非常に重要なテーマである。今回の研究は、その新たな治療法を示唆する基礎研究である。細胞膜が不安定な場合（膜コレステロール含量が減少した場合）には、AT1受容体構造の変化とAng IIが結合可能なAT1受容体発現量の減少が起こり、Ang IIによるIP産生能が低下し、血圧上昇と脈拍数増加が抑制され、心血管保護へ働く可能性が示唆されたとういことである。
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Report
(4 results)
Research Products
(2 results)
