Fig. 4: Lipodomic profiling after a burn injury reveals upregulation of ER stress inducing lipids.
From: Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction

a, b Heat map display of lipid species within the plasma taken from burn patients and post-burn mice. c Quantification of FFAs (Palimitic and Stearic) in the plasma of wild type burned mice and controls. d Immunoblot of ER stress marker p-eif2a in HepG2 cells exposed to vehicle or Palimitate (100 μm or 500 m) for 24 h. e Oxygen Consumption Rate (OCR) in HepG2 cells exposed to vehicle or Palimitate (500μm) for 24 h. f Quantitative RT-PCR analysis of ER stress/UPR gene expression from livers of wild type (WT) burned mice and controls. g Immunoblot analysis of ER stress/UPR proteins in liver samples of wild type (WT) burned mice and controls. h, i Quantitative RT-PCR analysis ER stress/UPR and CPEB4 gene expression from the livers of UCP-1−/− and IL-6−/− burned mice and controls. j Parametric analysis of gene-set enrichment (PAGE) of the most highly upregulated (red) and down-regulated (blue) mitochondrial genes in livers of wild type (WT) burned mice and controls. k Quantitative RT-PCR analysis of beta-oxidation genes in the livers of wild type (WT) burned mice and controls. Data represented as mean ± SEM, p < 0.05 *significant difference WT burn vs. controls (n = 8, biological replicates, experiments repeated two times).