Project/Area Number |
21390243
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Kyushu University |
Principal Investigator |
AGO Tetsuro 九州大学, 大学病院, 助教 (30514202)
|
Research Collaborator |
SADOSHIMA Junichi UMDNJ-New Jersey Medical School, Department of Cell Biology and Molecular Medicine, Professor
KURODA Junya 九州大学, 大学病院, 助教 (70614858)
ARIMURA Koichi 九州大学, 大学院・医学研究院, 大学院生
NISHIMURA Ataru 九州大学, 大学院・医学研究院, 大学院生
|
Project Period (FY) |
2009 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2011: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2009: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
|
Keywords | 酸化ストレス / レドックス / Nox4 / NADPH oxidase / 内皮細胞 / 脳虚血 / 血管新生 / ミトコンドリア / endothelial cell / pericyte / brain infarction / ischemia / mitochondria / hypoxia / 酸化ストレス/レドックス / 活性酸素種 / NADPH oxidase, Nox4 / 心血管病 / 脳梗塞 / 血管内皮細胞 / 血管周皮細胞(ペリサイト) / トランスジェニックマウス / 活性酸素種(ROS) / 一酸化窒素合成酵素 / NADPH oxidase,Nox4 / 高血圧 / 心不全 / 動脈硬化 |
Research Abstract |
Reactive oxygen species (ROS) play an important role in the development and progression of cardiovascular diseases. In the present study, we focused on the ROS-producing enzyme Nox4 expressed in endothelial cells. While the expression of Nox4 was suppressed under normal conditions, it was highly induced in micro-vessels in ischemic tissues, reinforced hypoxic responses, and increased the production of angiogenic and inflammatory molecules. The physiological role of Nox4 may be angiogenesis; however, the angiogenic responses induced by rapid induction of Nox4 may rather worsen the disease state under particular conditions, such as brain ischemia.
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