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*
Department of Biochemistry, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, and
Neurotoxicology Laboratories, Rutgers University College of Pharmacy, Piscataway, NJ 08854
Renal ischemia/reperfusion (I/R) injury is a major cause of kidney
damage. There is accumulating evidence that inflammatory reactions are
involved in the pathogenesis of this process. Our studies demonstrate
that transgenic mice overexpressing human extracellular and
intracellular glutathione peroxidases (GP) are protected against kidney
I/R injury. Importantly, significant reduction in neutrophil migration
was observed in GP mice compared with nontransgenic mice. Analysis of
signaling molecules mediating neutrophil activation and recruitment
indicates reduction in the level of KC and macrophage inflammatory
protein-2 chemokine expression in transgenic animals. The molecular
mechanism mediating this effect appears to involve repression of
NF-
B activation at the level of IB
and IBß degradation.
In the case of IB, no apparent phosphorylation was detected.
These results suggest that IB proteolysis is triggered during the
renal I/R pro-oxidant state by a still unknown mechanism, which might
be different from other stimuli. A central role of NF-B in CXC
chemokine activation was demonstrated in cell culture anoxia/ATP
repletion experiments as a model of I/R. The data presented indicate
the important role of GP-sensitive signal transduction pathways in the
development of inflammatory response and tissue injury during
I/R.
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