Attenuation of renal ischemia–reperfusion injury by postconditioning involves adenosine receptor and protein kinase C activation

  1. Shady M. Eldaif1,
  2. Jeremiah A. Deneve1,
  3. Ning-Ping Wang3,
  4. Rong Jiang1,
  5. Mario Mosunjac2,
  6. Christopher J. Mutrie1,
  7. Robert A. Guyton1,
  8. Zhi-Qing Zhao3,
  9. Jakob Vinten-Johansen1

Article first published online: 2 SEP 2009

DOI: 10.1111/j.1432-2277.2009.00949.x

Issue

Transplant International

Transplant International

Volume 23, Issue 2, pages 217–226, February 2010

Additional Information

How to Cite

Eldaif, S. M., Deneve, J. A., Wang, N.-P., Jiang, R., Mosunjac, M., Mutrie, C. J., Guyton, R. A., Zhao, Z.-Q. and Vinten-Johansen, J. (2010), Attenuation of renal ischemia–reperfusion injury by postconditioning involves adenosine receptor and protein kinase C activation. Transplant International, 23: 217–226. doi: 10.1111/j.1432-2277.2009.00949.x

Author Information

  1. 1

     Division of Cardiothoracic Surgery, Department of Surgery, Emory University School of Medicine and Carlyle Fraser Heart Center Cardiothoracic Research Laboratory, Emory Crawford Long Hospital, Atlanta, GA, USA

  2. 2

     Department of Surgical Pathology, Emory University School of Medicine and Carlyle Fraser Heart Center Cardiothoracic Research Laboratory, Emory Crawford Long Hospital, Atlanta, GA, USA

  3. 3

     Department of Biomedical Sciences, Mercer University School of Medicine, Savannah, Georgia, USA

*Jakob Vinten-Johansen PhD, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center of Emory Crawford Long Hospital, 550 Peachtree Street NE, Atlanta, Georgia 30308-2225, USA. Tel.: 404-686-2511; fax: 404-686-4888; e-mail: jvinten@emory.edu

Publication History

  1. Issue published online: 22 DEC 2009
  2. Article first published online: 2 SEP 2009
  3. Received: 24 April 2009 Revision requested: 20 May 2009 Accepted: 30 July 2009

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Keywords:

  • adenosine;
  • apoptosis;
  • postconditioning;
  • renal ischemia;
  • reperfusion injury

Summary

Significant organ injury occurs after transplantation and reflow (i.e., reperfusion injury). Postconditioning (PoC), consisting of alternating periods of reperfusion and re-occlusion at onset of reperfusion, attenuates reperfusion injury in organs including heart and brain. We tested whether PoC attenuates renal ischemia–reperfusion (I/R) injury in the kidney by activating adenosine receptors (AR) and protein kinase C (PKC). The single kidney rat I/R model was used. Groups: (1) sham: time-matched surgical protocol only. In all others, the left renal artery (RA) was occluded for 45 min and reperfused for 24 h. (2) Control: I/R with no intervention at R. All antagonists were administered 5 min before reperfusion. (3) PoC: I/R + four cycles of 45 s of R and 45 s of re-occlusion before full R. (4) PoC + ARi: PoC plus the AR antagonist 8-ρ-(sulfophenyl) theophylline (8-SPT). (5) PoC + PKCi: PoC plus the PKC antagonist chelerythrine (Che). In shams, plasma blood urea nitrogen (BUN mg/dl) at 24 h averaged 23.2 ± 5.3 and creatinine (Cr mg/dl) averaged 1.28 ± 0.2. PoC reduced BUN (87.2 ± 10 in Control vs. 38.8 ± 9, P = 0.001) and Cr (4.2 ± 0.6 in Control vs. 1.5 ± 0.2, P < 0.001). 8-SPT and Che reversed renal protection indices after PoC. I/R increased apoptosis, which was reduced by PoC, which was reversed by 8-SPT and Che. Postconditioning attenuates renal I/R injury by adenosine receptor activation and PKC signaling.

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