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Cytological transformations associated with parietal cell stimulation: critical steps in the activation cascade
B J Agnew1, J G Duman, C L Watson
1Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
Journal of Cell Science
|July 22, 1999
Summary
Rabbit parietal cells reveal how HCl secretion involves H, K-ATPase tubulovesicle recruitment. Inhibitors block vacuole swelling by preventing proton pump or protein redistribution, supporting the membrane recycling hypothesis.
Area of Science:
- Cell Biology
- Physiology
- Gastroenterology
Background:
- Parietal cells secrete hydrochloric acid (HCl) via a complex process involving the proton pump H, K-ATPase.
- Understanding the morphological changes during HCl secretion is crucial for identifying therapeutic targets.
Purpose of the Study:
- To investigate the morphological responses of cultured rabbit parietal cells to activators and inhibitors of HCl secretion.
- To localize key proteins like H, K-ATPase and ezrin during secretion.
- To evaluate the membrane recycling/recruitment hypothesis of HCl secretion.
Main Methods:
- Cultured rabbit parietal cells were treated with secretagogues and inhibitors.
- Immunofluorescence microscopy was used to visualize H, K-ATPase, ezrin, and F-actin.
- Morphological changes, including apical vacuole swelling and protein localization, were analyzed.
Main Results:
- Secretagogues caused apical vacuole swelling, which was blocked by various inhibitors.
- Inhibitors preventing H, K-ATPase tubulovesicle translocation maintained resting morphology.
- ME-3407 uniquely prevented H, K-ATPase redistribution and ezrin delocalization.
- Inhibitors of H+ pump or H+ backflux allowed translocation but diminished vacuole swelling.
Conclusions:
- Data support the membrane recycling/recruitment hypothesis for HCl secretion.
- The findings are inconsistent with models where tubulovesicles are contiguous with the apical plasma membrane.
- The parietal cell culture model is effective for distinguishing inhibitor mechanisms.