Fig. 6: A cell permeant IP3R peptide attenuates ER stress and blocks apoptosis in vitro.
From: Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction

a A schematic illustrating the consequences of increased hepatic ER stress and MAM enrichment that can lead to an efflux of excessive Ca2+ from the ER via the IP3R receptor to the mitochondria. The by-product of mitochondrial damage (cytochrome c) feedbacks to the IP3R to sustain this cycle that ultimately results in cellular apoptosis. b Immunoblot of ER stress proteins c-ATF6 and p-jnk in HepG2 cells treated with either TG (100 nM) for 24 h or vehicle. c Immunofluorescence staining of ER stress marker BiP (red) in HepG2 cells treated with either TG (100 nM) for 24 h or vehicle. d Immunoblot and quantification of ER stress protein p-eif2α from HepG2 cells treated with either TG (100 nM) for 24 h, TG (100 nM) treated cells incubated with either BODIPY-IP3RCYT-MUT(400 nM), and or BODIPY-IP3R-CYT(400 nM) for 4 h. e Immunofluorescence staining of pro-apoptotic marker CHOP (green) in HepG2 cells treated with either TG (100 nM) for 24 h, TG (100 nM) treated cells incubated with either BODIPY-IP3RCYT-MUT(400 nM), and or BODIPY-IP3RCYT(400 nM) for 4 h. f Quantification of Immunofluorescence staining of CHOP from (e). g Immunofluorescence staining of mitochondria with Deep Red MitoTracker (red) in HepG2 cells treated with either TG (100 nM) for 24 h, TG (100 nM) treated cells incubated with either BODIPY-IP3RCYT-MUT(400 nM), and or BODIPY-IP3RCYT(400 nM) for 4 h. h Quantification of Immunofluorescence staining of the MitoTracker from (g). Data represented as mean ± SEM, *p < 0.05 vs. control or TG, ϕp < 0.05 vs. control #p < 0.05 vs. IP3RCYT-MUT/ TG (n = 7, biological replicates, experiments repeated two times). Scale bars represent ×20 magnification for (c, e), and ×60 magnification for (g).