p53-cyclophilin D mediates renal tubular cell apoptosis in ischemia-reperfusion-induced acute kidney injury.

p53-cyclophilin D mediates renal tubular cell apoptosis in ischemia-reperfusion-induced acute kidney injury. Am J Physiol Renal Physiol. 2019 Jul 24;: Authors: Yang H, Li R, Zhang L, Zhang S, Dong W, Chen Y, Wang W, Li C, Ye Z, Zhao X, Li Z, Wu Y, Zhang M, Liu S, Dong Z, Liang X Abstract Ischemia-reperfusion-induced acute kidney injury (IR-AKI) favors mitochondrial permeability transition pore (mPTP) opening and subsequent cell death. Cyclophilin D (CypD) is an essential component of the mPTP, and recent findings implicate the p53-CypD complex in cell death. To evaluate the role of p53-CypD following IR-AKI, we tested the hypothesis that the p53-CypD complex mediates renal tubular cell apoptosis in IR-AKI via mPTP opening. The expression of p53 and cleaved caspase-3 was significantly increased in rats subjected to IR-AKI compared with the normal control and sham-operated control. The underlying mechanisms were determined using an in vitro model of ATP-depletion. The inhibition of mPTP opening using the CypD inhibitor cyclosporin A or a siRNA for p53 in ATP-depleted HK-2 cells prevented mitochondrial membrane depolarization and reduced apoptosis. Furthermore, p53 binds to CypD in ATP-depleted HK-2 cells. These results suggest that the p53-CypD complex mediates renal tubular cell apoptosis in IR-AKI via mPTP opening. PMID: 31339772 [PubMed - as supplied by publisher]
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research

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