| Project/Area Number |
24591057
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kagawa University |
|---|
Principal Investigator |
OHMORI Koji 香川大学, 医学部, 准教授 (00263913)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HASAN Arif Ul 香川大学, 医学部, 研究員 (00570368)
KOHNO Masakazu 香川大学, 医学部, 教授 (20153489)
NOMA Takahisa 香川大学, 医学部附属病院, 講師 (20363202)
IMACHI Hitomi 香川大学, 医学部, 准教授 (80380187)
ISHIHARA Yasuhiro 香川大学, 医学部附属病院, 助教 (80532689)
HORII Taiko 香川大学, 医学部, 教授 (90423425)
YAMASHITA Yoichi 香川大学, 医学部, 准教授 (80363208)
|
|---|
| Project Period (FY) |
2012-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| 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: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 動脈硬化 / 肥満 / 脂肪細胞 / 血管内皮成長因子 / アディポサイトカイン / vasa sasorum / 細胞培養 / レポーターアッセイ / 血管内皮細胞増殖因子 / n-3系長鎖必須脂肪酸 / Gタンパク質共役受容体120 / インターロイキン6 / アンジオテンシン受容体遮断薬 / PPAR-γ / 低酸素 / メタボリックシンドローム / アンジオテンシン受容体 / 炎症 / 血管新生 / レニンアンジオテンシン系 / 腫瘍抑制因子 / 多価不飽和脂肪酸 |
|---|
| Outline of Final Research Achievements |
It is hypothesized that periarterial adipose tissue releases vascular endothelial growth factor (VEGF) and proinflammatory cytokines into vascular wall from adventitial side to grow the atherosclerotic plaques. In this study employing mature adipocytes, block of constitutive activity of angiotensin II type-1 receptor by valsartan decreased production of interleukin-6 and increased that of adiponectin. However, another putative anti-atherosclerotic fatty acid, eicosapentaenoic acid promoted the production of VEGF through an integrated mechanism including G-protein coupled receptor 120 and peroxisome-proliferator activated receptor-gamma. These findings provide for the comprehensive understanding of the "out-side-in" mechanisms for atherosclerosis.
|
