Establishment of a new diagnostic method for antiphospholipid antibody syndrome and elucidation of pathogenic mechanism
Project/Area Number |
26860370
|
Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Laboratory medicine
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Research Institution | Yamaguchi University |
Principal Investigator |
MOTOKI Yukari 山口大学, 医学(系)研究科(研究院), 助教 (80724054)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
|
Keywords | 抗リン脂質抗体症候群 / 抗リン脂質抗体 / 血栓症 / 酸化ストレス / 動脈血栓症 / 動脈硬化 |
Outline of Final Research Achievements |
Antiphospholipid syndrome (APS) is an autoimmune disease characterized by arterial and/or venous thrombosis associated with antiphospholipid antibodies. IgG from APS patients and anti-phosphatidylserine/prothrombin antibody (aPS/PT) increased expression of tissue factor (TF) and production of chemokines from endothelial cells (EC). Oxidative stress level was significantly higher in sera of APS patients than in those of healthy subjects. Treatment with oxidative stress led to increase in expression of TF, chemokines, but decrease in the expression of eNOS of EC. The decrease in eNOS leads to a decrease in production of NO, and anti-arteriosclerotic effect by NO might be decreased. It is suggested that the decrease of NO and increase of TF, proinflammatory cytokine and chemokines are cause of thrombosis in APS patients. In the examination of APS, measurement of anti-cardiolipin antibody (aCL) -IgG is the first test item, followed by measurements of aPS/PT-IgG and aCL-IgM are recommended.
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Report
(4 results)
Research Products
(9 results)