| Project/Area Number |
26293230
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Partial Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Collagenous pathology/Allergology
|
|---|
| Research Institution | Hokkaido University |
|---|
Principal Investigator |
Tatsuya Atsumi 北海道大学, 医学(系)研究科(研究院), 教授 (20301905)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
奥 健志 北海道大学, 大学病院, 助教 (70544295)
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2016: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2015: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
|
|---|
| Keywords | 内科 / 免疫学 / 脂質 / 生体分子 / 内科学 |
|---|
| Outline of Final Research Achievements |
We have strived to develop novel APS animal model using arteriosclerotic mouse model with additional monoclonal aPL administration, however, failed to develop the spontaneous thrombosis.
Recently, we have clarified that abnormal acceleration of the complement activation contributes to APS pathogenesis and the autoantibody against first component of the classical pathway (C1q), highly produced in the patients' sera, initiates the activation. Additionally, in APS, primary abnormality of the vascular endothelial cells,especially dysfunction of endothelial NOS(eNOS) secretion is reported.These factors facilitates aPL to bind the cell surfaces of vascular endothelial cells via inducing anionic phospholipids expressions on cell membranes. And these processes result to the up-regulation of pro-thrombotic states of the cells.We are now planning to establish APS model mouse by using eNOS KO mouse with the pathogenic autoantibodies (aPL, anti-C1q antibody) which seems promising
|
