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. 2017 Aug 3;8(46):80545–80559. doi: 10.18632/oncotarget.19849

Figure 3. Targeting UPR signaling components differentially regulate cellular metabolism.

Figure 3

(A) RAW 264.7 macrophage cells were transfected with control, GRP78, IRE1, or PERK siRNA for 24 hours, and then treated with or without LPS. Intracellular lipids were stained for oil-red-o and representative images obtained at 40×. (B) UPR signaling components IRE1, PERK, and GRP78 in RAW 264.7 cells were inhibited by RNAi treatment for 24 hours followed by treatment with 1 μg/mL LPS for 24 hours. ATGL was measured by Western blot hybridization. Protein loading was normalized to β-actin. (C) Glucose uptake in RAW 264.7 cells transfected with scrambled control or UPR targeting siRNA for 24 hours. n = 3; *p < 0.05. (D) Mitochondrial metabolomics was determined in transfected RAW 264.7 macrophages using a Seahorse Bioanalyzer. (E) Basal ECAR rates in transfected RAW 264.7 macrophage cells. n = 3–4; *p < 0.05.