Figure 3 from Single-Cell RNA Sequencing Unifies Developmental Programs of Esophageal and Gastric Intestinal Metaplasia

<p>Columnar cells of the stomach and esophageal IM have mosaic gastric and intestinal phenotypes. <b>A,</b> UMAP of columnar cells isolated from samples of NSCJ, NGC, NGB, ND, ileum, colon, rectum, BE, gastric metaplasia of esophagus, squamocolumnar junction between NE and BE, CIM, GIM, nonchronic atrophic gastritis, and chronic atrophic gastritis with color denoting cell types. The cell types were assigned using cells from normal tissue types. <b>B,</b> Scatter plot of log-normalized expression of intestinal (<i>GPA33</i>) and gastric (<i>MUC5AC</i>) markers in the selected tissue types. <b>C,</b> Coimmunofluorescent staining of the esophagus with BE with BE-IM and GIM shows coexpression of intestinal and gastric markers in both types of IM using lineage markers MUC5AC (gastric) and GPA33 (intestinal), and progenitor markers MUC6 (gastric) and OLFM4 (intestinal). White arrowheads denote selected goblet cells; dashed white lines indicate selected BE-IM and GIM crypts, for GIM samples: 1, a crypt with mixed gastric and intestinal phenotype; 2, a crypt with cells showing mosaic phenotype; 3, a crypt with features of complete IM; scale bar, 100 μm. See supplementary Figs. S8 and S9 for ND and NGC. Images are representative of 12 patients (NGC = 2, ND = 2, BE-IM = 4, and GIM = 4). <b>D,</b> UMAP with MuSiC-derived contribution of gastric and intestinal phenotypes to individual cells of the esophageal IM (top) and stomach IM (bottom). <b>E,</b> Violin plots of squamous, SMG, gastric, or intestinal phenotype contribution to cells from NGC, E-GM, BE-IM, BSCJ, NAG, CAG, GIM, CIM, and ND samples.</p>