Regulation of gastric epithelial cell development revealed in H+/K+-ATPase β-subunit- and gastrin-deficient mice

American Journal of Physiology - Gastrointestinal and Liver Physiology - Tập 281 Số 6 - Trang G1502-G1511 - 2001
Teo V. Franic1, Louise M. Judd1, David Robinson1, Simon P. Barrett1, Katrina L. Scarff1, Paul A. Gleeson1, Linda C. Samuelson2, Ian R. van Driel1
1Department of Pathology and Immunology, Monash University Medical School, Alfred Hospital, Melbourne, Victoria, Australia 3181; and
2Department of Physiology, University of Michigan, Ann Arbor, Michigan 48109-0622

Tóm tắt

The gastric H+/K+-ATPase is essential for normal development of parietal cells. Here we have directly assessed the role of the H+/K+-ATPase β-subunit (H/K-β) on epithelial cell development by detailed quantitation of the epithelial cell types of the gastric mucosa of H/K-β-deficient mice. H/K-β-deficient mice had a 3.1-fold increase in the number of immature cells per gastric unit; however, the numbers of surface mucous and parietal cells were similar to those in the gastric units of wild-type mice. The effect of elevated gastrin levels in the H/K-β-deficient mice was determined by producing mice that are also deficient in gastrin. We demonstrated that the increased production of immature cells and resulting hypertrophy is caused by the overproduction of gastrin. However, the depletion of zymogenic cells, which is another feature of H/K-β-deficient mice, is independent of hypergastrinemia. Significantly, parietal cells of H/K-β- and gastrin-deficient mice had abnormal secretory membranes and were devoid of resting tubulovesicular membranes. Together these data suggest a homeostatic mechanism limiting the number of immature cells that can develop into end-stage epithelial cells and indicate a direct role for H/K-β in the development of mature parietal cells.

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American Journal of Physiology - Gastrointestinal and Liver Physiology

Tập 281 Số 6

G1502-G1511

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