Elucidation of pathogenesis and progression mechanisms of glomerulonephritis through prostaglandin E2-renal dendritic cell axis
| Project/Area Number |
25860692
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Nippon Medical School |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 腎局在樹状細胞 / プロスタグランジンE2 (PGE2) / 腎疾患 / PGE2 / PDCA1 / DC / 樹状細胞 |
|---|
| Outline of Final Research Achievements |
I showed the novel phenotype of renal dendritic cell (RDC), CD11c+F4/80+PDCA1+. Furthermore, RDCs expressed PGE2 receptor as well as Cox-2 and mPGES-1 molecule involved in prostaglandin E2 synthesis which is known as an inflammatory mediator. These findings suggested that RDC function might be regulated by PGE2 autocrine manner.
In in vivo experiment, the population of RDCs in UUO (unilateral ureteral obstruction) mouse kidney were decreased, in which model is known that PGE2 expression is upregulated. However, the expressions of MHC classII molecule, IL-12/23p40 and IL-23p19 were significantly increased in RDCs migrated in UUO kidney.
|
Report
(3 results)
Research Products
(3 results)
