Abstract
ObjectiveParietal cell‐expressed Sonic Hedgehog (Shh) regulates function and differentiation of the gastric epithelium. Correlative evidence shows that loss of Shh expression associated with Helicobacter pylori infection results in the disruption of the normal gastric epithelium. We sought to identify whether Shh regulates gastric epithelial cell differentiation in the absence of inflammation.MethodsA parietal cell‐specific, tamoxifen‐inducible deletion of Shh mouse model was developed (HKCreInd/ShhKO). Epithelial cell proliferation and migration was studied using BrdU and Ki67 co‐immunostaining. Cell lineage changes were studied using markers specific for surface mucous (Ulex europaeus, UEAI), mucous neck (Griffonia simplicifolia, GSII) and zymogen (intrinsic factor, IF) cells.ResultsCompared to Controls, HKCreInd/ShhKO mice developed foveolar hyperplasia reflected by an expansion of BrdU/UEAI positive cells. HKCreInd/ShhKO mice also showed an expansion of GSII/IF co‐expressing cells at the base of the gastric gland. Co‐localization of BrdU and Ki67 revealed loss of normal migration of the epithelial cells within HKCreInd/ShhKO mouse stomachs.ConclusionLoss of Shh in the adult stomach results in the development of foveolar hyperplasia and delayed differentiation of the zymogenic cell lineage independent of inflammation.(DHC Pilot and Feasibility Project Award, Zavros)
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