| Project/Area Number |
20790584
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Asahikawa Medical College |
|---|
Principal Investigator |
NAKAGAWA Naoki Asahikawa Medical College, 医学部, 特任助教 (10451460)
|
|---|
| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2008: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 腎臓学 / 再生医療 / 腎不全 / プロスタノイド |
|---|
| Research Abstract |
We have recently reported that the mice of the specific deletion of prostaglandin I2 receptor (IP) in bone marrow cells is used as endothelial progenitor cells (EPCs) dysfunction model. We investigated the condition is whether the renal failure worsened, using the mice of the specific deletion of IP in bone marrow cells (BMCs). We examined renal function and histological change in models of renal artery ischemia-reperfusion, ureteral ligation, and renal nephrectomy. Among the three models, in renal artery ischemia-reperfusion model, the serum creatinine levels were tend to higher, but no significant, in mice of the specific deletion of IP in BMCs compared with mice of the transfused wild-type EPCs in BMCs.
In the future, we will investigate the ischemic conditions in increasing the number of animals, and examine the changes in functional analysis, as well as ureteral ligation model and nephrectomy model. Furtheremore, we will clarify the role of the EPCs in the pathophysiology in kidney failure and the effect of injection of high functional EPCs in kidney failure.
|
