| Project/Area Number |
20790762
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|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
|---|
| Research Field |
Pediatrics
|
|---|
| Research Institution | National Research Institute for Child Health and Development |
|---|
Principal Investigator |
MAKIKO Nakayama National Research Institute for Child Health and Development, 腎臓科, 客員臨床研究員 (80469999)
|
|---|
| Project Period (FY) |
2008 – 2009
|
| Project Status |
Completed (Fiscal Year 2009)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2008: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 小児難治性ネフローゼ / リツキシマブ / B細胞 |
|---|
| Research Abstract |
Potentiated generation of reactive oxygen spices (ROS) from neutrophil Nox2 by TNF-α was reported to contribute to ICAM-1 expression in vascular endothelial cells (VEC), which plays a key role in neutrophil extravasation and following aneurysm formation. However, this possibility was only concluded by indirect studies using reducing agents or inhibitors against Nox. In order to get a definite answer, we produced a mouse model of Kawasaki disease using LCWE, and then inspected it with Nox2-KO mice. The inspection studies clearly demonstrated that TNF-α induces ICAM-1 expression, directly affecting VEC without the aid of ROS from neutrophil Nox2.
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