Genetic delineation of the pathways mediated by bid and JNK in tumor necrosis factor-alpha-induced liver injury in adult and embryonic mice.

ABSTRACT: Tumor necrosis factor-alpha (TNFalpha)-induced hepatocyte death and liver injury can be mediated by multiple mechanisms, which could be evaluated by different animal models. Previous studies have defined the importance of Bid in mitochondrial apoptosis activation in adult mice treated with lipopolysaccharides in the presence of galactosamine (GalN), which suppresses NF-kappaB activation, but not in embryonic mice in which NF-kappaB activation is suppressed by genetic deletion of p65RelA. JNK has also been found important in TNFalpha-induced mitochondria activation and liver injury in the lipopolysaccharide/GalN and concanavalin A (ConA)/GalN models, but not in a ConA-only model in which NF-kappaB activation was not suppressed. To determine the mechanistic relationship of pathways mediated

SUBMITTER: Ni HM 

PROVIDER: S-EPMC2640960 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature