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J Am Soc Nephrol. 2011 Oct;22(10):1887-96. doi: 10.1681/ASN.2011010031. Epub 2011 Aug 12.

Bβ(15-42) attenuates the effect of ischemia-reperfusion injury in renal transplantation.

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  • 1Department of Nephrology and Hypertension, Medical School Hannover, Germany.


Renal ischemia-reperfusion contributes to reduced renal allograft survival. The peptide Bβ(15-42), a breakdown product of fibrin, attenuates inflammation induced by ischemia-reperfusion in the heart by competitively blocking the binding of leukocytes to endothelial VE-cadherin, but whether it could improve outcomes in renal transplantation is unknown. Here, we tested the ability of Bβ(15-42) to ameliorate the effects of renal ischemic injury during allogenic kidney transplantation in mice. In our renal transplantation model (C57BL/6 into BALB/c mice), treatment with Bβ(15-42) at the time of allograft reperfusion resulted in significantly improved survival of recipients during the 28-day follow-up (60% versus 10%). Bβ(15-42) treatment decreased leukocyte infiltration, expression of endothelial adhesion molecules, and proinflammatory cytokines. Treatment significantly attenuated allogenic T cell activation and reduced cellular rejection. Moreover, Bβ(15-42) significantly reduced tubular epithelial damage and apoptosis, which we reproduced in vitro. These data suggest that Bβ(15-42) may have therapeutic potential in transplant surgery by protecting grafts from ischemia-reperfusion injury.

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