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Am J Physiol Gastrointest Liver Physiol (July 17, 2002). doi:10.1152/ajpgi.00515.2001
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Articles in PresS, published online ahead of print July 17, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00515.2001
Submitted on December 7, 2001
Accepted on July 9, 2002

Role of NF-{kappa}B on Liver Cold Ischemia/Reperfusion Injury

Yoshihito Takahashi1, Raymond W. Ganster1, Andrea Gambotto1, Lifang Shao1, Takashi Kaizu1, Tong Wu2, Gautam P. Yagnik1, Atsunori Nakao1, George Tsoulfas1, Takashi Ishikawa1, Toyokazu Okuda1, David A. Geller1, and Noriko Murase1*

1 Department of Surgery, University of Pittsburgh, Thomas E. Starzl Transplantation Institute, Pittsburgh, PA, USA
2 Department of Pathology, University of Pittsburgh, Pittsburgh, PAS, USA

* To whom correspondence should be addressed. E-mail: murase+{at}pitt.edu.

The role of NF-{kappa}B, the rapid response transcription factor for multiple genes, in cold ischemia/reperfusion (I/R) injury was examined after syngenic transplantation of liver grafts. Lewis rat recipients were sacrificed 1-48 hours after reperfusion of three different liver grafts: 1) uninfected control, 2) infected ex-vivo with control adenoviral vector (AdEGFP), and 3) infected ex-vivo with AdI{kappa}B. In uninfected control livers, NF-{kappa}B was activated biphasically at 1-3 hours and 12 hours after reperfusion with AST levels of 4244±691 IU/L. The first peak of NF-{kappa}B activation associated with an increase of mRNA for TNF-{alpha}, IL1-ß and IL-10. AdEGFP-transfection resulted in similar outcomes. Interestingly, AdI{kappa}B-transfected liver grafts suffered more severe I/R injury (AST >9000 IU/L). Transfected I{kappa}B was detected in transplanted livers as early as 6 hours, and this correlated with the abrogation of the second, but not the first, peak of NF-{kappa}B activation at 12-48 hours and increased apoptosis. Thus, inhibition of the second wave of NF-{kappa}B activation in I{kappa}B transfected livers resulted in an increase of liver injury, suggesting that NF-{kappa}B may have a dual role during liver I/R injury.




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