CYLD deletion triggers nuclear factor-κB-signaling and increases cell death resistance in murine hepatocytes

Figure 2 Decreased liver injury in CYLD^-/- mice after D-galactosamine/lipopolysaccharide and Jo2 treatment. A: Box-plots of serum transaminases alanine aminotransferase (ALT) (left panel) and aspartate aminotransferase (AST) (right panel) levels 5 h after D-galactosamine (D-GalN)/lipopolysaccharide (LPS) injection. n = 10 vs 10; B: Western blot analysis of caspase and Bid activation in pooled liver lysates from D-GalN/LPS treated WT and CYLD^-/- mice; C: Caspase-3 activity assays of pooled liver lysates from D-GalN/LPS treated WT and CYLD^-/- mice. Caspase-3 substrate turnover was measured by fluorometric analysis at the indicated time points; D: WT mice showed more single cell necrosis and apoptosis compared to CYLD^-/- mice (HE). Representative immunohistological stainings of cl. PARP (Scale bar: 40 μm) and quantification of cl. PARP positive nuclei. Values represent the mean ± SD; E: Box plots of serum transaminases ALT (left panel) and AST (right panel) levels 3 h after Jo2 injection. n = 10 vs 10; F: Western blot analysis of caspase and Bid activation in pooled liver lysates from Jo2 treated WT and CYLD^-/- mice. (G) Caspase-3 activity assays of pooled liver lysates from Jo2 treated WT and CYLD^-/- mice. Caspase-3 substrate turnover was measured by fluorometric analysis at the indicated time points; H: Liver cell damage was increased in WT compared to CYLD^-/- (HE). Representative immunohistological stainings of cl. PARP (Scale bar: 40 μm) and quantification of cl. PARP positive nuclei. Values represent the mean ± SD. ^aP < 0.05, WT vs CYLD^-/-; ^bP < 0.01, WT vs CYLD^-/-; ^dP < 0.01, WT vs CYLD^-/-.