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Effects of a gastrin receptor antagonist (NTZ, previously named YF) on the gastric corpus mucosa of HKATPase betasubunit knockout (KO) mice

ABSTRACT: Purpose: the effects of a gastrin receptor antagonist has been studies in patients with gastrin neuroendocrine (NE) tumours due to hypergastrinemia. This mouse model of hypergastrinemia is a model for studying long term acid inhibition, including NE hyperplasia and formation of Spasmolytic polypeptide expressing metaplasia (SPEM), a proposed premalignant alteration of the stomach. Methods: RNA was isolated from the oxyntic mucosa. RNA was sequenced using standard Illumina protocols on a NextSeq 500 instrument. Results: NTZ reduced oxyntic mucosal hypertropohy and stomach weight. Neuroendocrine cell hyperplasia and NE markers were also reduced. Spasmolytic polypeptide expressing metaplasia (SPEM) was expressed in KO mice and was not affected by the gastrin receptor antagonist. Conclusions: The gastrin receptor antagonist YF reduced gastric corpus mucosal hypertrophy and NE cell hyperplasia in HKATPase KO mice, but did not affect SPEM or SPEM related genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE142513 | GEO | 2019/12/23

REPOSITORIES: GEO

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Endogenous glucocorticoids suppress spontaneous gastric inflammation and spasmolytic polypeptide expressing metaplasia

Project description:Adrenalectomy induced severe eosinophil and macrophage infiltration localized to the gastric corpus resulting in development of spasmolytic polypeptide expressing metaplasia (SPEM) and oxyntic atrophy. RNA sequencing analysis revealed significant upregulation of proinflammatory genes 3 days post-adrenalectomy, prior to leukocyte infiltration and histopathological changes.

2019-03-20 | GSE107736 | GEO

Tristetraprolin prevents gastric metaplasia by suppressing pathogenic inflammation

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2021-11-10 | GSE164349 | GEO

IL-33 regulates metaplasia and macrophage polarization in the stomach.

Project description:Alternatively-activated macrophages (M2) are known to play a critical role in intestinalization of spasmolytic polypeptide-expressing metaplasia (SPEM), which is a precursor to gastric adenocarcinoma. However, the precise mechanism(s) and critical mediators produced by M2 macrophages that lead to SPEM are unknown. Using established murine models of metaplasia in the stomach, the aim of the present study was to determine how M2 macrophages induce intestinalized SPEM. Macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced intestinalized SPEM (L635-treated) were isolated and RNA sequencing was performed. IL-33 was the most upregulated cytokine in macrophages associated with intestinalized SPEM. L635-treated IL-33 knock out mice did not develop metaplasia, suggesting that IL-33 is required for the induction of SPEM after acute parietal cell loss. While the loss of IL-33 did not reduce macrophage recruitment into the mucosa, infiltrating macrophages were not M2 polarized. We conclude that IL-33 is necessary for both the induction of mucous metaplasia (SPEM) in the stomach and polarization towards M2 in recruited macrophages. Our data suggest that the inflammatory pathway in the stomach after parietal cell loss resembles pathways associated with allergy-induced airway inflammation, which implicates novel treatment options for gastritis patients to prevent gastric cancer.

2017-01-20 | GSE77195 | GEO

Transplantation of gastric organoid-derived spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) cell lineage promotes ulcer repair in the aged stomach

Project description:Background & Aims: Spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) is known to emerge following parietal cell loss and during Helicobacter pylori infection, however its role in gastric ulcer repair is unknown. Therefore, we sought to investigate if SPEM plays a role in epithelial regeneration. Methods: Acetic acid ulcers were induced in young (2-3 months) C57BL/6 mice to determine the quality of ulcer repair. Gastric tissue was collected and analyzed to determine the expression of SPEM within the regenerating epithelium. As a comparison to native tissue the expression of SPEM was also identified within cultured gastric mouse-derived organoids. Results: Wound healing in the mice coincided with the emergence of SPEM expressing CD44v within the ulcerated region. The emergence of SPEM was also observed in cultured gastric organoids. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. 4 samples were used for ulcerated and uninjured tissue. 1 sample was used for intact tissue and organoid-derived RNA. The 'Ulcerated' samples represent C57BL/6 mice with ulcers and the 'Uninjured' samples represent the healthy controls (for "ulcerated" samples). The "Intact stomach tissue" and "Gastric organoids" samples are other types of samples that compared separately. "Gastric organoids" in this comparison are derived from "Intact stomach tissue".

2015-09-23 | E-GEOD-73336 | biostudies-arrayexpress

Expression data from acutely damaged stomachs

Project description:Tamoxifen injection injures the mouse stomach, triggering a plastic regenerative response termed Spasmolytic Polypeptide Exressing Metaplasia. We are probing how tamoxifen treated stomachs differ from healthy controls, and also how injected rapamycin affects this process

2018-02-15 | GSE103570 | GEO

Protein Kinase A (PKAc alpha ) regulates gastric homeostasis and preneoplastic lesions

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Transcriptional analysis reveals the molecular details of atrophic gastritis in Helicobacter pylori infected corpus mucosa

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2014-02-04 | E-GEOD-27411 | biostudies-arrayexpress

Transplantation of gastric organoid-derived spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) cell lineage promotes ulcer repair in the aged stomach

2015-09-23 | GSE73336 | GEO

Transcriptional analysis reveals the molecular details of atrophic gastritis in Helicobacter pylori infected corpus mucosa

2014-02-04 | GSE27411 | GEO

Gastric Myofibroblasts Control Chief Cell differentiation, and their recovery from SPEM

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