| Project/Area Number |
24591107
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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 | Iwate Medical University (2013-2014)
Tohoku University (2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
GAO Junhong 東北大学, 大学院医学系研究科, 助教 (70455781)
SHOUJIROU Sawada 東北大学, 大学院医学系研究科, 助教 (60509420)
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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 |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 動脈硬化 / 小胞体ストレス / 酸化ストレス |
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| Outline of Final Research Achievements |
The interactions among biological pathways, such as responses to inflammation, oxidative stress and endoplasmic reticulum (ER) stress are thought to be important for the development of atherosclerosis. Wolfram Syndrome (WFS) 1, which regulates ER stress response genes, is expressed in vascular endothelial cells, smooth muscle cells and macrophages. Cuff injury-induced vascular remodeling and hypercholesterolemia-induced aortic plaque formation were markedly advanced in WFS1-/- mice with exacerbated aortic expressions of inflammatory factors and oxidative stress markers. The results of studies in vitro revealed that WFS1 directly modulate inflammatory and oxidative stress response in vascular cells as well as macrophage. Thus, WFS1 may play important roles in suppressing potentially pathological biological stress responses, resulting in prevention of atherosclerosis.
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