New mechanisms for organ damage elucidated by oxidative stress associated with innate immunity
| Project/Area Number |
24591115
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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 | Yamaguchi University |
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Principal Investigator |
UMEMOTO Seiji 山口大学, 医学部附属病院, 准教授 (90263772)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Koichi 山口大学, 大学院医学系研究科, 准教授 (00322248)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | hypertension / Toll-like receptor 4 / organ damage / ecSOD / angiotensin / inflammation / MCP-1 / vascular remodeling / angiotensin II |
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| Outline of Final Research Achievements |
We examined the relationships among Toll-like receptor 4 (TLR4), angiotensin II (AngII), NADPH oxidase-derived oxidative stress, antioxidant enzyme extracellular superoxide dismutase (ecSOD), and inflammation in organ damage in AngII-induced hypertension. We demonstrated that TLR4 plays a pivotal role in regulating AngII-induced oxidative stress levels by inhibiting the expression and activity of the antioxidant enzyme ecSOD, as well as by activating NADPH oxidase, which enhances inflammation induced by monocyte/macrophage infiltration to facilitate selectively activated MCP-1 and the progression of organ damage seen in AngII-induced hypertension.
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Report
(4 results)
Research Products
(8 results)
