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1 Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA, USA
2 Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA
3 Department of Physiology, Medical College of Georgia, Augsuta, GA, USA
4 Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA, USA; Medical Research Service, Veterans Affairs Medical Center, Augusta, GA, USA
* To whom correspondence should be addressed. E-mail: zdong{at}mail.mcg.edu.
Tubular cell apoptosis is involved in ischemic renal failure, but the underlying mechanism is unclear. Bid, a pro-apoptotic Bcl-2 family protein, may regulate the intrinsic as well as the extrinsic pathway of apoptosis. In vivo, Bid is most abundantly expressed in the kidneys. However, the role played by Bid in renal patho-physiology is unknown. Our recent work demonstrated Bid activation during renal ischemia-reperfusion. The current study has determined the role of Bid in ischemic renal injury and renal failure using Bid-deficient mice. In wild-type C57BL/6 mice, Bid was proteolytically processed into active forms during renal ischemia-reperfusion, which subsequently targeted mitochondria. This was accompanied by the development of tissue damage and severe renal failure, showing serum creatinine of 3.0 mg/dl after 48 hours of reperfusion. The same ischemic insult induced acute renal failure in Bid-deficient mice, which was nonetheless less severe than the wild-type, showing 1.3 mg/dl serum creatinine. In addition, Bid-deficiency attenuated tubular disruption, tubular cell apoptosis and caspase-3 activation during 48 hours of reperfusion. Compared with the wild-type, animal death following renal ischemia was delayed in Bid-deficient mice. Collectively, the results suggest a role for Bid in ischemic renal injury and renal failure.
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