2014 Fiscal Year Final Research Report
role of p21 activation and senescence on acute kidney injury
| Project/Area Number |
25860190
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General pharmacology
|
|---|
| Research Institution | Kagawa University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Keywords | 急性腎障害 / 細胞周期 / p21 |
|---|
| Outline of Final Research Achievements |
We investigated the role of p21 in acute kidney injury and ischemic preconditioning (IPC). Mice lacking p21 (p21-KO) and wild-type mice underwent renal ischemia followed by reperfusion (I/R). I/R increased p21 expression in the kidneys. The acute kidney injury was worse in p21-KO mice than in wild-type mice. The results suggest that p21 confers tolerance to I/R injury. IPC attenuated I/R injury in wild-type mice, but not in p21-KO mice. IPC decreased the number of proliferating tubular cells before I/R and increased it at 24 h after I/R in the kidney of wild-type mice. In p21-KO mice, IPC did not change the number of proliferating cells before I/R, and decreased it after I/R. IPC increased renal p21 expression and the number of cells in the G1 phase of the cell cycle before I/R. In conclusion, renal p21 is essential for the beneficial effects of renal IPC.
|
| Free Research Field |
薬理学
|
