| 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)
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| 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.
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