Differential activation pattern of redox-sensitive transcription factors and stress-inducible dilator systems heme oxygenase-1 and inducible nitric oxide synthase in hemorrhagic and endotoxic shock

Abstract

These data suggest that AP-1 but not NF-kappaB activation is dependent on reactive oxygen intermediates in vivo and contributes to HO-1 gene expression. Thus, AP-1-dependent HO-1 induction under oxidative stress conditions may subserve a similar function as a stress-inducible vasodilator system as does NF-kappaB-dependent iNOS expression in liver inflammation.