| Project/Area Number |
20590256
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
IWATA Kazumi Kyoto Prefectural University of Medicine, 医学研究科, 講師 (60305571)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUNO Harukuni 京都府立医科大学, 医学研究科, 助教 (50420708)
KAKEHI Tomoko 京都府立医科大学, 医学研究科, プロジェクト研究員 (20433279)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2008: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 原発性肺高血圧症 / 活性酸素 / NADPH oxidase / 活性酸素種 / NOX1 / 遺伝子欠損マウス / 肺動脈平滑筋細胞 |
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| Research Abstract |
Pulmonary arterial hypertension is characterized by hypertrophy of small pulmonary arteries, which leads to right ventricular (RV) hypertrophy and heart failure. Nox1 is a catalytic subunit of NADPH oxidase known as a major source of superoxide production in vascular tissues. In Nox1-defcient mice (Nox1-/Y) hypertrophy of small pulmonary arteries and RV wall were observed. A significant decrease in number of apoptotic cells were demonstrated in pulmonary arterial smooth muscle cells (PASMC) isolated from Nox1-/Y. Dysfunction of Kv1.5, a voltage-dependent potassium channel, is one of the features reported in human and experimental PAH. A significant decrease in Kv1.5 protein and an increase in intracellular potassium levels were observed in Nox1-/Y PASMC.These results suggest that Nox1 plays a critical role in apoptosis of PASMC by regulating Kv1.5 expression and intracellular potassium levels.
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