ArticleCarcinogenesis2011
Cox-2 deletion in myeloid and endothelial cells, but not in epithelial cells, exacerbates murine colitis.
Article in Carcinogenesis, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Eosinophil-derived COX-2 protects against experimental colitis through the PGEbioRxiv : the preprint server for biology · 2025Article
- Dynamic changes in macrophage populations and resulting alterations in Prostaglandin ECell communication and signaling : CCS · 2025Article
- Validate the Treatment of Crohn's Disease with Chaihu Guizhi Decoction Through Network Pharmacology, Molecular Dynamics Simulation, and in vivo Experiments.Journal of inflammation research · 2025Article
- Estrogen deprivation and estrogen receptor α antagonism decrease DSS colitis in female mice.Pharmacology research & perspectives · 2024Article
- Microbial-Dependent Recruitment of Immature Myeloid Cells Promotes Intestinal Regeneration.Cellular and molecular gastroenterology and hepatology · 2024Article
- 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
- ApoA-I mimetics favorably impact cyclooxygenase 2 and bioactive lipids that may contribute to cardiometabolic syndrome in chronic treated HIV.Metabolism: clinical and experimental · 2021Article
- Effects of Genetic and Pharmacologic Inhibition of COX-2 on Colitis-associated Carcinogenesis in Mice.Journal of cancer prevention · 2020Article
- Slco2a1 deficiency exacerbates experimental colitis via inflammasome activation in macrophages: a possible mechanism of chronic enteropathy associated with SLCO2A1 gene.Scientific reports · 2020Article
- Eicosanoid signaling in carcinogenesis of colorectal cancer.Cancer metastasis reviews · 2018Review
- mPGES-1-Mediated Production of PGEFrontiers in immunology · 2018Article
- HIF-1α Deletion in the Endothelium, but Not in the Epithelium, Protects From Radiation-Induced Enteritis.Cellular and molecular gastroenterology and hepatology · 2018Article
- Cysteinyl leukotriene receptor 1 facilitates tumorigenesis in a mouse model of colitis-associated colon cancer.Oncotarget · 2017Article
- Niacin ameliorates ulcerative colitis via prostaglandin DEMBO molecular medicine · 2017Article
- Phospholipase Cϵ Activates Nuclear Factor-κB Signaling by Causing Cytoplasmic Localization of Ribosomal S6 Kinase and Facilitating Its Phosphorylation of Inhibitor κB in Colon Epithelial Cells.The Journal of biological chemistry · 2016Article
- Contribution of alveolar type II cell-derived cyclooxygenase-2 to basal airway function, lung inflammation, and lung fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Eicosanoid pathway in colorectal cancer: Recent updates.World journal of gastroenterology · 2015Review
- A reporter mouse for optical imaging of inflammation in mdx muscles.Skeletal muscle · 2015Article
- The Hen or the Egg: Inflammatory Aspects of Murine MPN Models.Mediators of inflammation · 2015Review
- Targeted deletion and lipidomic analysis identify epithelial cell COX-2 as a major driver of chemically induced skin cancer.Molecular cancer research : MCR · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Patients with inflammatory bowel diseases are at increased risk for colorectal cancer. Pharmacological inhibition of cyclooxygenase (COX) function exacerbates symptoms in colitis patients. Animal models of colitis using Cox-2-knockout mice and COX inhibitors also indicate that COX-2 has a protective role against colon inflammation. However, because conventional Cox-2 deletion and COX-2 inhibitors eliminate COX-2 function in all cells, it has not been possible to analyze the role(s) of COX-2 in different cell types. Here, we use a Cox-2(flox) conditional knockout mouse to analyze the role of COX-2 expression in distinct cell types in the colon in response to dextran sulfate sodium (DSS)-induced colitis. We generated Cox-2 conditional knockouts in myeloid cells with LysMCre knock-in mice, in endothelial cells with VECadCreERT2 transgenic mice and in epithelial cells with VillinCre transgenic mice. When treated with DSS to induce colitis, both myeloid cell-specific and endothelial cell-specific Cox-2-knockout mice exhibited greater weight loss, increased clinical scores and decreased epithelial cell proliferation after DSS injury when compared with littermate controls. In contrast, epithelial-specific Cox-2 knockouts and control littermates did not differ in response to DSS. These results suggest that COX-2 expression in myeloid cells and endothelial cells, but not epithelial cells, is important for protection of epithelial cells in this murine colitis model.
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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.