ArticleGastroenterology2014
Macrophages promote progression of spasmolytic polypeptide-expressing metaplasia after acute loss of parietal cells.
Article in Gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 133 citations in OpenAlex.
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Diet-Induced Obesity ExacerbatesbioRxiv : the preprint server for biology · 2026Article
- Gastric Microbiota Dysbiosis and Microbiome-Based Interventions in Chronic Atrophic Gastritis.Nutrients · 2026Review
- Gastric intestinal metaplasia: unraveling the multifactorial pathogenesis and advancing risk stratification for gastric cancer prevention.Cellular and molecular life sciences : CMLS · 2026Review
- Regulation of STK38 by autophagy governs YAP1 activity during paligenosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Multimerin1 and not Galectin-8 tempers WNT signaling to promote gastric chief cell differentiation.Scientific reports · 2026Article
- Research progress on the correlation between OPN and immune escape of gastric cancer.Clinical and experimental medicine · 2026Review
- Recent advances in spasmolytic polypeptide expressing metaplasia research.World journal of gastrointestinal oncology · 2026Review
- Roles of interleukins in spasmolytic polypeptide‑expressing metaplasia (Review).International journal of oncology · 2026Review
- Multimerin1, not Galectin-8, Promotes Gastric Chief Cell Differentiation by Tempering WNT Signaling.bioRxiv : the preprint server for biology · 2025Article
- Pyroptosis in gastric mucosal injury‑related diseases (Review).International journal of molecular medicine · 2025Review
- Cathartocytosis: Jettisoning of cellular material during reprogramming of differentiated cells.Cell reports · 2025Article
- Cellular lineage origins of spasmolytic polypeptide-expressing metaplasia (SPEM): persistent and intensifying debates.Frontiers in oncology · 2025Review
- The role of the S100A8/S100A9 in gastric tumor progression.Scientific reports · 2024Article
- Endogenous glucocorticoids are required for normal macrophage activation and gastricAmerican journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Regulation of metaplasia and dysplasia in the stomach by the stromal microenvironment.Experimental & molecular medicine · 2024Review
- Oncogenic Fatty Acid Metabolism Rewires Energy Supply Chain in Gastric Carcinogenesis.Gastroenterology · 2024Article
- Autoimmune Atrophic Gastritis: A Clinical Review.Cancers · 2024Review
- Role and research progress of spasmolytic polypeptide‑expressing metaplasia in gastric cancer (Review).International journal of oncology · 2024Article
- The Importance of Th2 Immune Responses in Mediating the Progression of Gastritis-Associated Metaplasia to Gastric Cancer.Cancers · 2024Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsLoss of parietal cells causes the development of spasmolytic polypeptide-expressing metaplasia (SPEM) through transdifferentiation of chief cells. In the presence of inflammation, SPEM can advance into a more proliferative metaplasia with increased expression of intestine-specific transcripts. We used L635 to induce acute SPEM with inflammation in mice and investigated the roles of inflammatory cells in the development of SPEM.
methodsTo study the adaptive immune system, Rag1 knockout, interferon-γ-deficient, and wild-type (control) mice received L635 for 3 days. To study the innate immune system, macrophages were depleted by intraperitoneal injection of clodronate liposomes 2 days before and throughout L635 administration. Neutrophils were depleted by intraperitoneal injection of an antibody against Ly6G 2 days before and throughout L635 administration. Pathology and immunohistochemical analyses were used to determine depletion efficiency, metaplasia, and proliferation. To characterize SPEM in each model, gastric tissues were collected and levels of Cftr, Dmbt1, and Gpx2 mRNAs were measured. Markers of macrophage polarization were used to identify subpopulations of macrophages recruited to the gastric mucosa.
resultsAdministration of L635 to Rag1 knockout, interferon-γ-deficient, and neutrophil-depleted mice led to development of proliferative SPEM and up-regulation of intestine-specific transcripts in SPEM cells, similar to controls. However, macrophage-depleted mice given L635 showed significant reductions in numbers of SPEM cells, SPEM cell proliferation, and expression of intestine-specific transcripts, compared with control mice given L635. In mice given L635, as well as patients with intestinal metaplasia, M2 macrophages were the primary inflammatory component.
conclusionsResults from studies of mouse models and human metaplastic tissues indicate that M2 macrophages promote the advancement of SPEM in the presence of inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.