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. 2021 Mar 3;12(2):395–425. doi: 10.1016/j.jcmgh.2021.02.013

Figure 3.

Figure 3

H pylori induces Rev-erbα expression via the phosphorylated cagA-activated ERK signaling pathway. (A, B) AGS cells were pretreated with signal pathway inhibitors and then stimulated with WT H pylori (MOI = 100) for 24 hours. Rev-erbα mRNA expression in AGS cells was compared (n = 3). (C) AGS cells were stimulated with WT H pylori with different MOI (6 hours) or at different time point (MOI = 100). ERK1/2 and p-ERK1/2 proteins were analyzed by Western blot. (D) AGS cells were pretreated with or without U0126 and then infected with WT H pylori or ΔcagA (MOI = 100) for 24 hours. Rev-erbα mRNA expression in these cells was compared (n = 3). Rev-erbα, ERK1/2, and p-ERK1/2 proteins were analyzed by Western blot. (E) AGS cells were transfected with plasmids pcDNA3.1 or cagA-pcDNA3.1 for 24 hours, then treated with or without U0126 for 2 hours and cultured for an additional 24 hours. Rev-erbα mRNA expression in these cells was compared (n = 3). Rev-erbα, ERK1/2, and p-ERK1/2 proteins were analyzed by Western blot. (F) AGS cells were pretreated with or without PP2 and then infected with WT H pylori or ΔcagA (MOI = 100) for 24 hours. Rev-erbα mRNA expression in these cells was compared (n = 3). Rev-erbα, ERK1/2 and p-ERK1/2 proteins were analyzed by Western blot. ∗P < .05, ∗∗P < .01, n.s. P > .05 for groups connected by horizontal lines.