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. Author manuscript; available in PMC: 2019 Aug 29.
Published in final edited form as: Gastroenterology. 2019 Mar 1;156(8):2158–2173. doi: 10.1053/j.gastro.2019.02.036

Figure 3.

Figure 3.

Modeling changes in the cytoskeleton at the apical membranes of gastric parietal cells. Model of VacA-induced hypochlorhydria. In resting cells, apical microvilli are supported by microfilaments that extend deep into the cytoplasm. Ezrin (red dots) links actin filaments with the apical plasma membrane. Histamine stimulation leads to docking and fusion of ATP4A-rich tubulovesicles to the apical plasma membrane, expanding the apical surface. Interactions between the apical membrane and microfilaments, via ezrin, reorganize the expanded surface into long microvilli. VacA induces proteolysis of ezrin, disrupting the interactions between the apical membrane and microfilaments, and preventing recruitment of ATP4A to the apical membrane. The ensuing parietal cell inability to secrete acid results in hypochlorhydria.