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. 2020 Dec 18;14(3):303–311. doi: 10.21053/ceo.2020.01907

Fig. 4.

Fig. 4.

E-cigarette vapor (with or without nicotine)-induced MUC5AC expression in human nasal epithelial cells is associated with ERK1/2, p38, and NF-κB activation. (A) Immunofluorescence results showing that e-cigarette vapor without nicotine significantly induced MUC5AC expression, and this was significantly inhibited by pretreatment with U0126 (an ERK1/2 inhibitor), SB203580 (a p38 inhibitor), or BAY 11-7085 (an NFκB inhibitor). E-cigarette vapor without nicotine also significantly increased MUC5AC expression in the cytoplasm. Each bar shows the mean± standard deviation of three independent experiments. (B) Immunofluorescence results showing that e-cigarette vapor with nicotine significantly increased MUC5AC expression, and this was significantly inhibited by pre-treatment with U0126 (an ERK1/2 inhibitor), SB203580 (a p38 inhibitor), or BAY 11-7085 (an NF-κB inhibitor). Furthermore, e-cigarette vapor with nicotine significantly increased MUC5AC expression in the cytoplasm. Con, control; e-cigarette, electronic cigarettes; DAPI, 4ʹ,6-diamidino-2-phenylindole; ERK, extracellular signal-regulated kinase; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells.