Innate immunity regulation by prothymosin alpha -mimetics
| Project/Area Number |
25670061
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Environmental and hygienic pharmacy
|
|---|
| Research Institution | Nagasaki University |
|---|
Principal Investigator |
UEDA Hiroshi 長崎大学, 医歯薬総合研究科(薬学系), 教授 (00145674)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUNAGA Hayato 長崎大学, 医歯薬総合研究科(薬学系), 客員研究員 (20437833)
TANAKA Yoshimasa 長崎大学, 医歯薬総合研究科(薬学系), 准教授 (90280700)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | DAMPs / 生理活性物質 / 受容体 / スクリーニング / プロサイモシンα / TLR4 / プライミング / 網膜虚血 / ハイスループットスクリーニング / 自然免疫 / 神経創薬 / ペプチドミメティクス |
|---|
| Outline of Final Research Achievements |
Prothymosin alpha; (ProTa) is a robustness protein, which inhibits brain ischemia (injury) -induced neuronal and vascular damages. Using retinal ischemia model in mice, we found that preconditioning treatment with ProTa blocks microglia-mediated neuroinflammation in experiments using histological, electrophysiological and expressed gene analyses. We also clarified the underlying mechanisms through an activation of TLR4-mediated TRIF-IRF3 pathway, but not of MyD88-NFkB pathway. Furthermore, in order to search for small compounds possessing similar beneficial compounds, we successfully developed TLR4-mediated IRF3-responsive reporter assay system based on secretary alkaline-phosphatase activity in HEK293 cells.
|
Report
(4 results)
Research Products
(10 results)
