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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 919313, 9 pages
Research Article

Nrf2 Is Crucial to Graft Survival in a Rodent Model of Heart Transplantation

1Department of Pharmacology and Toxicology, The University of Arizona, Tucson, AZ 85721, USA
2Department of Cardiothoracic Surgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, China
3Department of Pathology, School of Medicine, Northwestern University, Chicago, IL 60611, USA
4Department of Pathology, The University of Arizona, Tucson, AZ 85724, USA

Received 26 November 2012; Accepted 15 January 2013

Academic Editor: Jingbo Pi

Copyright © 2013 Wei Wu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Currently, the sole treatment option for patients with heart failure is transplantation. The battle of prolonging graft survival and modulating innate and adaptive immune responses is still being waged in the clinic and in research labs. The transcription factor Nrf2 controls major cell survival pathways and is central to moderating inflammation and immune responses. In this study the effect of Nrf2 levels in host recipient C57BL/6 mice on Balb/c allogeneic graft survival was examined. Importantly, Nrf2−/− recipient mice could not support the graft for longer than 7.5 days on average, whereas activation of Nrf2 by sulforaphane in Nrf2+/+ hosts prolonged graft survival to 13 days. Several immune cells in the spleen of recipient mice were unchanged; however, CD11b+ macrophages were significantly increased in Nrf2−/− mice. In addition, IL-17 mRNA levels were elevated in grafts transplanted into Nrf2−/− mice. Although Nrf2 appears to play a crucial role in graft survival, the exact mechanism is yet to be fully understood.