| Project/Area Number |
23700546
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Biomedical engineering/Biological material science
|
|---|
| Research Institution | Kawasaki Medical School |
|---|
Principal Investigator |
HASHIMOTO Ken 川崎医科大学, 医学部, 講師 (80341080)
|
|---|
| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 動脈硬化 / 血管内皮細胞 / 単球 / 逆浸潤 / TRPV2 / 内皮細胞 / 浸潤 / 血管内皮 |
|---|
| Research Abstract |
Pathophysiological significance of momocyte reverse transmigration from subendothelium back into the blood stream during atherogenesis is unclear. We established the quantitative evaluation system of reverse transmigration, and revealed that high dose of IL-1β selectively impaired the process. This suggests that in strong inflammatory conditions like atherosclerosis, the clearance activity of pathogenic substances in subendothelium is impaired due to suppressed reverse transmigration. Meanwhile, mechanical stimulations like membrane stretch are generated at the border of migrating monocytes and endothelial cells. We evaluated the role of TRPV2, previously reported mechano-sensitive cation channels, and demonstrated its necessity for cells to move.
|
