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Am J Physiol Gastrointest Liver Physiol 283: G1175-G1184, 2002. First published July 17, 2002; doi:10.1152/ajpgi.00515.2001
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Vol. 283, Issue 5, G1175-G1184, November 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

Thomas E. Starzl Transplantation Institute, Departments of 1 Surgery and 2 Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213

The role of NF-kappa B, the rapid-response transcription factor for multiple genes, in cold ischemia-reperfusion (I/R) injury was examined after syngeneic transplantation of liver grafts. Lewis rat recipients were killed 1-48 h 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 AdIkappa B. In uninfected control livers, NF-kappa B was activated biphasically at 1-3 and 12 h after reperfusion with aspartate transaminase (AST) levels of 4,244 ± 691 IU/l. The first peak of NF-kappa B activation associated with an increase of mRNA for TNF-alpha , IL-1beta , and IL-10. AdEGFP transfection resulted in similar outcomes. Interestingly, AdIkappa B-transfected liver grafts suffered more severe I/R injury (AST >9,000 IU/l). Transfected Ikappa B was detected in transplanted livers as early as 6 h, and this correlated with the abrogation of the second, but not the first, peak of NF-kappa B activation at 12-48 h and increased apoptosis. Thus inhibition of the second wave of NF-kappa B activation in Ikappa 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.

liver transplantation; preservation injuries; Ikappa B; adenoviral vector


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