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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: J Pathol. 2016 Jun 22;239(4):399–410. doi: 10.1002/path.4735

Figure 6. Schematic summary for progression of SPEM in gerbil gastric corpus following H. pylori 7.13 infection.

Figure 6

After H. pylori infection, SPEM is generated via transdifferentiation of chief cells following parietal cell loss, and then evolves into more progressive phenotypes with intestinal and invasive characteristics. MUC4 expression is upregulated in SPEM and then increases as SPEM progresses toward intestinal metaplasia. Clusterin is expressed in the bottom of SPEM glands, and the clusterin-positive regions give rise to aberrant gland phenotypes and invade into the submucosa.