Figure 2
From: GDF15 deficiency exacerbates chronic alcohol- and carbon tetrachloride-induced liver injury

Recombinant GDF15 enhances oxygen consumption in hepatocytes and inhibits the expression of pro-inflammatory cytokines in Kupffer cells. (a,b) Oxygen consumption rates were measured in primary murine hepatocytes treated with vehicle or recombinant GDF15 (rGDF15, 100 or 200 ng/mL). Oligomycin (2 µg/mL) and rotenone (1 µM) were used as mitochondrial OXPHOS inhibitors. CCCP (5 µM), a mitochondrial uncoupler, was used to measure maximal mitochondrial respiration. (c) Real-time PCR analysis of Kupffer cells treated with lipopolysaccharide (LPS; 10 ng/mL) and/or rGDF15 (50 or 100 ng/mL). (d) Schematic description of co-culturing Kupffer cells with hepatocytes. (e) Real-time PCR analysis of Kupffer cells co-cultured with WT or GDF15 KO hepatocytes in medium containing lipopolysaccharide (10 ng/mL). (f) Real-time PCR analysis of HSCs co-cultured with WT or GDF15 KO hepatocytes in medium containing lipopolysaccharide (10 ng/mL) for 3 hours. All data are representative of three independent experiments and are expressed as the mean ± SEM. *P < 0.05 and **P < 0.01, versus the corresponding controls.