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Articles in PresS, published online ahead of print May 22, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00085.2002
Submitted on February 27, 2002
Accepted on May 16, 2002
1 Institute for Surgical Research, University of Munich, Munich, Germany
* To whom correspondence should be addressed. E-mail: Krombach{at}icf.med.uni-muenchen.de.
Activation of poly(ADPribose)polymerase (PARP) mediates oxidative stress-induced cell injury. We tested the hypothesis that PARP contributes to ischemia-reperfusion (I/R) damage of the liver by triggering the mechanisms of microcirculatory failure. Leukocyte- and platelet-endothelial cell interactions as well as sinusoidal perfusion were analyzed by intravital fluorescence microscopy after lobar hepatic I/R (90min/30min) in C57BL/6x129/Sv wild-type (PARP+/+), and PARP-deficient mice (PARP-/-). Hepatic I/R induced leukocyte/platelet-endothelial cell interactions and tissue injury in PARP+/+ mice, as indicated by impaired sinusoidal perfusion and increased ALT/AST serum activities. In PARP-/- mice, however, the postischemic increase in the numbers of rolling/adherent leukocytes and platelets was significantly lower. In addition, I/R-induced translocation of CD62P as well as mRNA expression of CD62E, CD54, and CD106 were attenuated. The degree of perfusion failure was reduced and the increase in the ALT/AST activities was lower in PARP-/- as compared to PARP+/+ mice. We conclude that PARP contributes to hepatic microvascular injury by triggering the expression/translocation of adhesion molecules and modulating leukocyte/platelet-endothelial cell interactions.
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