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. 2022 May 10;8:257. doi: 10.1038/s41420-022-01026-0

Fig. 3. H. pylori augments AQP5 expression by upregulating ASCL1.

Fig. 3

A Veen map of the transcription factors binding AQP5 predicted by hTFtarget database and AQP5-related genes in microarray data GSE106656. B, ASCL1 expression in 14 gastritis patients and 7 IM patients in microarray data GSE106656. C Correlation between ASCL1 and AQP5 expression in microarray data GSE106656. D ASCL1 mRNA level in mouse gastric mucosa measured by RT-qPCR (n = 6). E, ASCL1 mRNA level in mouse primary GECs measured by RT-qPCR. F Enrichment of ASCL1 on the AQP5 promoter detected by ChIP assay. G The silencing efficiency of si-ASCL1-1 or si-ASCL1-2 as reflected by ASCL1 mRNA level in mouse primary GECs transduced with si-ASCL1-1 or si-ASCL1-2 measured by RT-qPCR. H The target relationship between ASCL1 and AQP5 verified by dual luciferase reporter assay. I ASCL1 mRNA level in H. pylori-infected mouse primary GECs transduced with si-ASCL1 measured by RT-qPCR. *p < 0.05, **p < 0.01. Data were shown as the mean ± standard deviation. Cell experiments were repeated three times independently. Comparisons of data between two groups were analyzed by independent sample t-test. One-way ANOVA with Dunnett’s post hoc test was applied for the comparison of data among multiple groups. The data between groups at different time points were compared by repeated measures ANOVA.