Figure 9.

Disruption of primary cilia on gastrin-expressing cells induced gastrin expression and antral hyperplasia. SF9 GLUTag cells were transfected with kif3a siRNA to disrupt primary cilia and then treated with recombinant SHH (400 ng/mL) or IL1β (10 ng/mL) for 24 hours. (A) Secreted gastrin peptide in conditioned media was determined by ELISA and (B) Gastrin mRNA levels were determined by qPCR. n = 5 experiments. ∗P < 0.05 relative to Con. ^#P < .05, ^###P < .001, ^####P < .0001. Horizontal lines represent the median and interquartile range. Primary cilia on G cells were disrupted by deleting kif3a in GastCreERT2/kif3a^FL/FL mice for up to 7 months. (C) Axonemes of primary cilia (arrows) in GastCreERT2/kif3a^FL/FL mice were identified by immunostaining for acetylated tubulin (Ac-TUB, red) and colocalized with gastrin (green) and E-cadherin (blue). Scale bars = 10 μm. (D) Serum gastrin levels were determined by ELISA over 7 months. n = 5 mice per time point. Horizontal lines represent the median and interquartile range. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001 relative to time point 0. (E) Representative hematoxylin and eosin images and immunofluorescent images of gastric antrum stained with gastrin antibody (green). Scale bars = 50 μm. (F) Antral GLI2 and GAPDH protein determined by Western blot. n = 3 mice per group at time point 7 months. H&E, hematoxylin and eosin.