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Editorial
. 2018 Mar;154(4):801-803.
doi: 10.1053/j.gastro.2018.02.001. Epub 2018 Feb 6.

Cellular Plasticity in the Stomach: Insights Into the Cellular Origin of Gastric Metaplasia

Elise S Hibdon  1 , Linda C Samuelson  2
Affiliations
Editorial

Cellular Plasticity in the Stomach: Insights Into the Cellular Origin of Gastric Metaplasia

Elise S Hibdon et al. Gastroenterology. 2018 Mar.
No abstract available

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1.
Figure 1.
Competing theories for the cellular origin of Spasmolytic Polypeptide-Expressing Metaplasia (SPEM) in the stomach. Schematic representation of gastric chief cell-derived (A) vs. progenitor cell-derived (B) SPEM. Under homeostatic conditions (left), the gastric corpus is maintained by actively cycling stem and progenitor cells that proliferate and differentiate into mature epithelial cell types. After injury that results in parietal cell loss and gastric atrophy, such as observed with Helicobacter pylori infection or tamoxifen treatment, corpus glands undergo cellular remodeling with loss of chief cells and rapid development of the metaplastic cell lineage termed SPEM. The cellular source of SPEM has been controversial due to differing interpretations of genetic lineage tracing data from analysis of Mist1-CreERT2 mice. In model A, SPEM is derived from transdifferentiation of mature MIST1+ chief cells. In model B, SPEM is derived from a slowly cycling MIST1+ progenitor cell that expands in response to injury. The Mills laboratory used a non-lineage tracing method to support Model A that SPEM arises from differentiated chief cells rather than a progenitor cell.
See this image and copyright information in PMC

Comment on

References

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