| Project/Area Number |
24790867
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | National Cardiovascular Center Research Institute |
|---|
Principal Investigator |
TSUDA Hidetoshi 独立行政法人国立循環器病研究センター, 研究所, 流動研究員 (40622618)
|
|---|
| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
|---|
| Keywords | 間葉系幹細胞 / 組織再生 / 免疫制御 / 虚血再灌流障害 / 卵膜 / 細胞治療 |
|---|
| Research Abstract |
We recently showed that fetal membrane-derived MSCs (FM-MSCs), which are available non-invasively in large amounts, had renoprotective effect in a glomerulonephritis model. Here, we investigated whether FM-MSCs administration could protect kidneys from ischemia/reperfusion (I/R) injury.Lewis rats were subjected to right nephrectomy and left renal I/R injury by clamping left renal artery. After declamping FM-MSCs were intravenously administered.I/R injured rats exhibited increased serum creatinine and BUN, whereas FM-MSCs ameliorated renal function. Histological analysis revealed that FM-MSCs suppressed tubular apoptosis and infiltration of macrophages and T cells. Administration of FM-MSCs mainly homed into lung, but increased serum IL-10 levels. Of interest is that renoprotective effects of FM-MSCs were abolished by using anti-IL-10 neutralization antibody, suggesting that IL-10 would be one of the candidate factors to protect rat kidney from I/R injury in this model.
|
