| Project/Area Number |
25670391
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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 |
Cardiovascular medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
ICHIKI Toshihiro 九州大学, 医学(系)研究科(研究院), 研究員 (80311843)
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| Co-Investigator(Renkei-kenkyūsha) |
SUNAGAWA Kenji 九州大学, 大学院医学研究院, 教授 (50163043)
KITAMOTO Shiro 九州大学, 大学院医学研究院, 講師 (00380436)
TOKUNOU Tomotake 九州大学, 大学院医学研究院, 助教 (50567378)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 低酸素応答系 / マイクログリア / 心肥大 / 圧負荷 / 室傍核 / PHD |
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| Outline of Final Research Achievements |
Microglia is considered brain macrophage and is involved in immune response in the brain. Although macrophages play an important role in the development of cardiovascular diseases, contribution of microglia is not clear. We sought to determine whether the hypoxia response system in microglia plays any roles in the development of pressure overload-induced cardiac hypertrophy.
We generated mice with macrophage-specific deletion of prolyl hydroxylase domain protein (PHD) 2 that induces degradation of hypoxia-inducible factor. Pressure overload by constriction of transverse aorta induced slightly less cardiac hypertrophy in PHD2-deficient mice. However, activation of microglia in the paraventricular nucleus, one of the nuclei that regulate sympathetic nerve activity, was not difference between PHD2-deficient and control mice. These results suggest that the hypoxia response system in microglia plays little role in the development of pressure overload-induced cardiac hypertrophy.
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