Molecular mechanisms of vascular inflammation induced by uremic toxins
Project/Area Number |
24591111
|
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 | Tokyo Medical and Dental University |
Principal Investigator |
YOSHIDA Masayuki 東京医科歯科大学, 生命倫理研究センター, 教授 (80282771)
|
Co-Investigator(Kenkyū-buntansha) |
OSAKA Mizuko 東京医科歯科大学, 生命倫理研究センター, 助教 (00581711)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2012: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 血管内皮細胞 / 炎症反応 / 心腎連関 / 血管生物学 / 慢性炎症 / 慢性腎臓病 / 尿毒症毒素 |
Outline of Final Research Achievements |
Indoxyl sulfate, a member of uremic toxins, significantly induces Ly6C-high monocytes recruitment to cuff-injured mouse femoral artery. These monocytes strongly express CCR2, suggesting a role forMCP-1 and CCR2 dependent signaling. Endothelial specific knock out mouse of AhR, a receptor of indoxyl sulfate, failed to exhibit indoxyl sulfate-induced monocyte recruitment.
|
Report
(4 results)
Research Products
(6 results)