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. 2017 Mar 24;292(20):8195–8206. doi: 10.1074/jbc.M116.769422

Figure 6.

Figure 6.

PGE2-mediated potentiation of LPS-stimulated IL-33 production is independent of p38 MAPK and NF-κB activation. A, effect of the p38 MAPK inhibitors SKF 86002 and SB706504 on IL-33 production by LPS (1.0 μg/ml) with or without PGE2. B, protein lysates from WT, mPGES-1 KO, and EP2 KO bmMFs 30 min after LPS stimulation were analyzed by WB, showing levels of phospho-p38 MAPK in WT, mPGES-1 KO, and EP2 KO bmMFs. C, IL-33 production by bmMFs in the presence of NF-κB inhibitor. D, NF-κB activation levels upon LPS stimulation in WT bmMFs in the presence of other selective agonists. E, WB analysis showing NF-κB activation by IκB phosphorylation in WT, mPGES-1 KO, and EP2 KO cells upon LPS stimulation and PGE2 addition. F, IL-33 levels with the ERK1/2 inhibitor FR180204 (1.0 μm) in the absence or presence of PGE2. G, effect of the JNK signaling inhibitor SP 600125 (100.0 μm) on IL-33 levels. Data are presented as mean ± S.E. of at least three independent experiments. Statistical significance was determined using one-sample t test (comparing fixed 100%). p < 0.05 was considered statistically significant. *, p < 0.05; **, p < 0.005.