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

Figure 1. Chemical UPR stressor agents differentially effects macrophage polarity.

Figure 1

(A) RAW 264.7 cells were pretreated with vehicle, 1 mM DTT, or 1 μg/mL tunicamycin (Tn) for 4 hours before treatment with 1 μg/mL LPS for 24 hours. GRP78, IRE1, and PERK were measured by Western blot hybridization. Protein loading was normalized to β-actin. n = 3; *p < 0.05. (B) RAW 264.7 cells were pretreated with vehicle, 1 mM DTT, or 1 μg/mL tunicamycin (Tn) for 4 hours before treated with 1 μg/mL LPS for 24 hours. iNOS and Arg-1 were measured by Western blot hybridization. Protein loading was normalized to β-actin. n = 3; *p < 0.05. (C) RT-PCR of iNOS, ARG-1, IL-6, IL-10, and IL-12 in RAW 264.7 cells pretreated with vehicle, 1 mM DTT, or 1 μg/mL tunicamycin (Tn) for 4 hours before treatment with 1 μg/mL LPS for 24 hours. Gene expression was normalized to the 18s housekeeping gene. n = 5; *p < 0.05. (D) 4T1 breast cancer cells were plated in an ACEA E-plate for 24 hours; RAW 264.7 macrophages pretreated with vehicle, 1 mM DTT, or 1 μg/mL Tn for 24 hours were then added to the E-plate. Each well was treated with 1 μg/mL LPS and the cell index was measured at 8 hours by electrical impedance. n = 3; *p < 0.05.