Gene expression profiles of starved mice and mice treat with TNF alpha

Pathogenesis of atherosclerosis results from the interactions between disrupted lipid homeostasis and immune response but the molecular bridges between the major players are still a matter of controversy. We investigated the systemic effect of inflammatory cytokine tumor necrosis factor alpha (TNF-α), a well established anorexia agent, in livers of mice exposed to 24h-cytokine/starvation. 10% of genes of the Agilent 10kb cDNA array is detected above level of detection in the mouse liver. 12% of these is modulated upon starvation while 22% is altered by TNF-α. Keywords: Disease state analysis Twelve mice (C57BL/6, Harlan) were randomly assigned into three groups. Three animals were i.v. injected by human recombinant TNF-α (30 µg/animal), a dose that is known to have a significant effect in mice without leading to mortality. Food was withdrawn after application of TNF-alpha (TNF/starvation group). Further, for three animals which were treated with corresponding volume (200µl) of saline a food was withdrawn (starvation group). Three animals from control group had free access to food throughout the study. Mice were sacrificed 20 hours later. Livers for RNA analysis were stored in RNAlater (Quiagen) according to manufacture's instruction. RNA of individual treated mouse was hybridized versus control sample which is obtained by pooling of control RNAs.