Fig. 6.

ER stress is associated with lipid accumulation in hepatocytes and suppression of β-oxidation gene expression. a Western blots showing levels of ER stress markers (cleaved ATF and CHOP) in hepatocytes. WT mice with and without treatment with ER stress inducer tunicamycin (TM; 2 μg/mL) for 6 h. GAPDH was used as a loading control. Images representative of at least three repeated experiments. Gray analyses was performed for quantization of protein expression. Three independent experiments were performed. All data are means ± SEM. *P < 0.05. b Western blots showing levels of ER stress markers (cleaved ATF and CHOP) in hepatocytes from HC-HMGB1-KO mice with and without treatment with ER stress inhibitor 4-phenylbutyric acid (PBA; 200 μM) for 12 h. c Lipid accumulation shown by Oil O Red Staining (red) in WT mouse hepatocytes treated with/without TM, or HC-HMGB1-KO mouse hepatocytes treated with/without PBA. x60 magnification. Representative images of multiple fields of view. Experiment repeated at least twice. d Relative gene expression of CPT-1α, MCAD, LCAD and VLCAD β-oxidation genes in WT mouse hepatocytes treated with/without TM; e Relative gene expression of CPT-1α, MCAD, LCAD and VLCAD β-oxidation genes in HC-HMGB1-KO mouse hepatocytes treated with/without PBA (n = 4 for each group). Data are expressed as mean ± SEM. *P < 0.05 between indicated groups. f Representative Western blot image of HMGB1, Cpt-1α and MCAD protein expression in whole cell lysates of WT and HC-HMGB1-KO hepatocytes at 40 h after transfection with control plasmid (ctrl) or plasmid expressing His-HMGB1. Quantification of relative protein expression shown below. Data presented as mean ± SEM. Data representative of at least three repeats. *P < 0.05 between indicated groups