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Endogenous glucocorticoids suppress spontaneous gastric inflammation and spasmolytic polypeptide expressing metaplasia

ABSTRACT: Endogenous glucocorticoids suppress spontaneous gastric inflammation and spasmolytic polypeptide expressing metaplasia

PROVIDER: PRJNA421214 | ENA |

REPOSITORIES: ENA

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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

Glucocorticoids and androgens suppress group 2 innate lymphoid cell activation and protect from pathogenic gastric inflammation and metaplasia

Project description:Glucocorticoids and androgens suppress group 2 innate lymphoid cell activation and protect from pathogenic gastric inflammation and metaplasia

| PRJNA613264 | ENA

Endogenous glucocorticoids prevent gastric metaplasia by suppressing spontaneous inflammation.

Project description: Not available

| S-EPMC6391099 | biostudies-literature

Tristetraprolin prevents gastric metaplasia by suppressing pathogenic inflammation

Project description:Purpose: The goals of this study are to examine whether TTP can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM). Methods: we utilized the TTP∆ARE mouse model to examine whether TTP overexpression can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM). Results: We found that TTP∆ARE mice were completely protected from ADX-induce gastric inflammation and SPEM. RNA sequencing revealed that TTP overexpression suppressed the expression of genes associated with the innate immune response. Finally, we show that protection from gastric inflammation was only partially due to suppression of Tnf, a well-known TTP target. Conclusions: Our results demonstrate that TTP exerts broad anti-inflammatory effects in the stomach, and suggest that therapies that increase TTP expression may be effective treatments of pro-neoplastic gastric inflammation.

2021-11-10 | GSE164349 | 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

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

Glucocorticoids suppress beta-cell development and induce hepatic metaplasia in embryonic pancreas.

Project description: Not available

| S-EPMC1223676 | biostudies-other

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

YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [RNA-Seq]

Project description:YAP is a transcriptional co-activator of the hippo signaling pathway and is known for its oncogenic and regenerative activity across numerous tissue types. In particular, high YAP levels in patients with gastric cancer (GC) confer a lower survival rate and poor prognosis for these individuals. Therefore, there is a great need to develop targeted therapies against these aggressive tumors. However, the role of YAP and its underlying molecular mechanisms during gastric tumorigenesis are still poorly understood. Using genetic models, we demonstrate the oncogenic function of YAP in CLU+ gastric cells in vivo. YAP over-expression in CLU+ cells induced atrophy, metaplasia and hyperproliferation in the gastric corpus, while its deletion in a Notch activated gastric tumor model rescued metaplasia. Furthermore, we defined the YAP1 targetome in YAP activated gastric tumors, and showed that YAP1 binds to the active chromatin elements of spasmolytic polypeptide-expressing metaplasia (SPEM) related genes and activates their expressions in gastric tumors and ulcers. Together, these results reveal YAP1 as a critical regulator of metaplasia in the gastric corpus, and highlights YAP signaling as a possible therapeutic target to inhibit the progression of gastric tumors.

2023-11-07 | GSE199171 | GEO

YAP-activated metaplasia underlies gastric adenocarcinoma and corpus regenerative mechanisms [ChIP-Seq]

2023-11-07 | GSE199170 | GEO

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