Fig. 5: Hepatic ER stress post-burn injury leads to increased ER-Mitochondrial interaction.
From: Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction

a, b Representative TEM images and quantification (scale bare = 100 nm) illustrating ER-Mitochondria tethering in liver sections derived from wild type (WT) burned mice and controls. c, d Representative PLA images (×63 magnification) and quantification of VDAC1/IP3R1 interactions (small red dots around the nucleus) in livers from wild type (WT) burned mice and controls. e Representative western blot and quantification of MAM enriched protein IP3R1 in livers of wild type (WT) burned mice and controls. f Representative TEM images (scale bare = 100 nm) illustrating ER-mitochondria tethering of liver sections derived Sham, Burn, and Tun + Burn mice. g Representative western blot of MAM enriched protein IP3R1 in livers of Sham, Burn, Tun., and Tun + Burn mice. h, i Representative PLA images (×63 magnification) and quantification of VDAC1/IP3R1 interactions (small red dots around the nucleus) in livers of Sham, Burn, Tun., and Tun + Burn mice. j Parametric analysis of gene-set enrichment (PAGE) of the most highly upregulated (red) and down-regulated (blue) mitochondrial genes in livers of burned mice and Tun + Burn mice. Data represented as mean ± SEM, p < 0.05 *significant difference WT burn vs. control, p < 0.05 # WT burn vs. Tun + Burn (n = 8, biological replicates, experiments repeated two times).