ArticleProstaglandins & other lipid mediators
The role of PGE2 in intestinal inflammation and tumorigenesis.
Article in Prostaglandins & other lipid mediators. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 96 citations in OpenAlex.
- Article
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- Differential susceptibility to colonic ulceration in mice with genetic deletion ofResearch square · 2025Article
- Hypothesizing mechanistic links between microbes and disease using knowledge graphs.Scientific reports · 2025Article
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- Mechanisms of Magnoliae Officinalis Cortex Volatile Oil in Alleviating 5-Fluorouracil-Induced Mucositis via Multi-Omics Approaches.Drug design, development and therapy · 2025Article
- Determination of nine prostaglandins in the arachidonic acid metabolic pathway with UHPLC-QQQ-MS/MS and application toFrontiers in pharmacology · 2025Article
- Microsomal Prostaglandin E Synthase-1 Controls Colonic Prostaglandin EInternational journal of molecular sciences · 2024Article
- PTGER4 signaling regulates class IIa HDAC function and SPINK4 mRNA levels in rectal epithelial cells.Cell communication and signaling : CCS · 2024Article
- Colonic Tuft Cells: The Less-Recognized Therapeutic Targets in Inflammatory Bowel Disease and Colorectal Cancer.International journal of molecular sciences · 2024Review
- Serine Supports Epithelial and Immune Cell Function in Colitis.The American journal of pathology · 2024Article
- Two genome-wide interaction loci modify the association of nonsteroidal anti-inflammatory drugs with colorectal cancer.Science advances · 2024Article
- Alveolar macrophage-derived gVPLA2 promotes ventilator-induced lung injury via the cPLA2/PGE2 pathway.BMC pulmonary medicine · 2023Article
- Prostaglandin E2 Exposure Disrupts E-Cadherin/Caveolin-1-Mediated Tumor Suppression to Favor Caveolin-1-Enhanced Migration, Invasion, and Metastasis in Melanoma Models.International journal of molecular sciences · 2023Article
- The Role and Mechanism of Retinol and Its Transformation Product, Retinoic Acid, in Modulating Oxidative Stress-Induced Damage to the Duck Intestinal Epithelial Barrier In Vitro.Animals : an open access journal from MDPI · 2023Article
- Macrophage orchestration of epithelial and stromal cell homeostasis in the intestine.Journal of leukocyte biology · 2022Review
- Possible cytoprotective mechanisms of oxytocin against 5-fluorouracil-induced gastrointestinal mucositis.Molecular biology reports · 2022Review
- Effects of Non-Polar Dietary and Endogenous Lipids on Gut Microbiota Alterations: The Role of Lipidomics.International journal of molecular sciences · 2022Review
- Facilitation of colonic T cell immune responses is associated with an exacerbation of dextran sodium sulfate-induced colitis in mice lacking microsomal prostaglandin E synthase-1.Inflammation and regeneration · 2022Article
- Tuft Cells and Their Role in Intestinal Diseases.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Release of the free fatty acid arachidonic acid (AA) by cytoplasmic phospholipase A2 (cPLA2) and its subsequent metabolism by the cyclooxygenase and lipoxygenase enzymes produces a broad panel of eicosanoids including prostaglandins (PGs). This study sought to investigate the roles of these mediators in experimental models of inflammation and inflammation-associated intestinal tumorigenesis. Using the dextran sodium sulfate (DSS) model of experimental colitis, we first investigated how a global reduction in eicosanoid production would impact intestinal injury by utilizing cPLA2 knockout mice. cPLA2 deletion enhanced colonic injury, reflected by increased mucosal ulceration and pro-inflammatory cytokine expression. Increased disease severity was associated with a significant reduction in the levels of several eicosanoid metabolites, including PGE2. We further assessed the precise role of PGE2 synthesis on mucosal injury and repair by utilizing mice with a genetic deletion of microsomal PGE synthase-1 (mPGES-1), the terminal synthase in the formation of inducible PGE2. DSS exposure caused more extensive acute injury as well as impaired recovery in knockout mice compared to wild-type littermates. Increased intestinal damage was associated with both reduced PGE2 levels as well as altered levels of other eicosanoids including PGD2. To determine whether this metabolic redirection impacted inflammation-associated intestinal tumorigenesis, Apc(Min/+) and Apc(Min/+):mPGES-1(-/-) mice were exposed to DSS. DSS administration caused a reduction in the number of intestinal polyps only in Apc(Min/+):mPGES-1(-/-) mice. These results demonstrate the importance of the balance of prostaglandins produced in the intestinal tract for maintaining intestinal homeostasis and impacting tumor development.
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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.