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. 2018 Mar 30;9(24):16678–16690. doi: 10.18632/oncotarget.24659

Figure 1. Chemerin activates NF-кB in HMEC-1 cells via MAPK and PI3K/Akt pathways; synergistic activation with IL-1β pathways.

Figure 1

Serum starved HMEC-1 cells stably transfected with pNFкB-Luciferase were treated with or without chemerin (0-10nM) for 2 hours. Cells were lysed and luciferase activities were measured. Chemerin induced a concentration dependent increase in luciferase activity after 2 hours of incubation (**P < 0.01 vs. basal, ***P < 0.001 vs. basal). When pre-incubated with BAY 11-7085 [(10μM), NF-ĸB inhibitor] or U0126 [(10μM), MAPK inhibitor] or SB202190 [(1 μM), p38 MAPK inhibitor] or LY294002 [(10 μM), PI3K/Akt inhibitor] for 1 hour, chemerin induced (10nM) NF-B activation was significantly attenuated (#P < 0.001 vs. chemerin (10nM) only treated). When chemerin (10nM) was co-incubated with IL-1β (0-100ng/mL), a significant increase in NF-B activity was observed [Figure 1: aP < 0.05, bP < 0.01, cP < 0.001 vs. IL-1β (100ng/mL) only treated, P < 0.001 vs. chemerin (10nM) only treated]. Data are mean ± SE of three experiments. Each experiment was carried out in three replicates. Group comparison by ANOVA (post hoc analysis: Tukey's test).