Assessment for abnormality of astrocyte in the sympathoexcitation of chronic heart failure
| Project/Area Number |
24591058
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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 |
Circulatory organs internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
KISHI Takuya 九州大学, 医学(系)研究科(研究院), 准教授 (70423514)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 循環器・高血圧 / 生理学 / 脳・神経 |
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| Outline of Final Research Achievements |
In the present research, I focused on brain astrocyte in sympathoexcitation of chronic heart failure. In the first 2 years, I evaluated neuron and astrocytes in rostral ventrolateral medulla, which is known as a vasomotor center in brainstem. In myocardial infarction-induced heart failure mice, astrocytes, not neurons, were reduced accompanied with apoptosis mediated by angiotensin II receptor and oxidative stress. In final year, we made astrocyte-specific angiotensin II type 1 receptor deletion mice using Cre-Lox P system, and determined that the survival of myocardial infarction-induced heart failure mice was significantly improved in astrocyte-specific angiotensin II type 1 receptor deletion mice.
These obtained results indicated that angiotensin II at astrocytes, not neuron, mainly cause abnormal sympathoexcitation in chronic heart failure, and that angiotensin II at astrocytes could be a novel therapeutic target in the treatment for chronic heart failure.
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Report
(4 results)
Research Products
(6 results)
