ArticlePloS one2013
Characterization of dextran sodium sulfate-induced inflammation and colonic tumorigenesis in Smad3(-/-) mice with dysregulated TGFβ.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- Targeted and quantitatively modeled biologic delivery via dual-functional probiotic yeast in inflammatory bowel disease.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- UC-associated autoantibodies to αvβ6 inhibit mucosal TGFβ activation and predispose to intestinal inflammation.bioRxiv : the preprint server for biology · 2026Article
- Gasdermin C links nutrient and immune signaling to protist-induced type 2 immunity and intestinal repair.bioRxiv : the preprint server for biology · 2025Article
- Stearoyl-CoA Desaturases regulate stem and progenitor cell metabolism and function in response to nutrient abundance.bioRxiv : the preprint server for biology · 2025Article
- Identifying Common Genetic Etiologies Between Inflammatory Bowel Disease and Related Immune-Mediated Diseases.Biomedicines · 2024Article
- Targeted delivery of the probiotic Saccharomyces boulardii to the extracellular matrix enhances gut residence time and recovery in murine colitis.Nature communications · 2024Article
- Effect of Carbamylated Erythropoietin in a Chronic Model of TNBS-Induced Colitis.Biomedicines · 2023Article
- The ADAM17 sheddase complex regulator iTAP/Frmd8 modulates inflammation and tumor growth.Life science alliance · 2023Article
- F4/80Gastroenterology · 2023Article
- Anti-Inflammatory Effect of Topiramate in a Chronic Model of TNBS-Induced Colitis.International journal of molecular sciences · 2022Article
- Transitional Anal Cells Mediate Colonic Re-epithelialization in Colitis.Gastroenterology · 2022Article
- Chronic Experimental Model of TNBS-Induced Colitis to Study Inflammatory Bowel Disease.International journal of molecular sciences · 2022Article
- Cancer-Associated Fibroblasts and Squamous Epithelial Cells Constitute a Unique Microenvironment in a Mouse Model of Inflammation-Induced Colon Cancer.Frontiers in oncology · 2022Article
- Evaluation of Pain and Distress and Therapeutic Interventions for Rectal Prolapse in Mice to Reduce Early Study Removal.Journal of the American Association for Laboratory Animal Science : JAALAS · 2021Article
- The Role of microRNAs in Development of Colitis-Associated Colorectal Cancer.International journal of molecular sciences · 2021Review
- Analysis of mutations in tumor and normal adjacent tissue via fluorescence detection.Environmental and molecular mutagenesis · 2021Article
- Genetic regulation and heritability of miRNA and mRNA expression link to phosphorus utilization and gut microbiome.Open biology · 2021Article
- Role of Eosinophils in Intestinal Inflammation and Fibrosis in Inflammatory Bowel Disease: An Overlooked Villain?Frontiers in immunology · 2021Review
- The Interaction Between the Microbiome and Tumors.Frontiers in cellular and infection microbiology · 2021Review
- Protective Effects of ALDH1A Enzyme Inhibition onNutrients · 2020Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are few mouse models that adequately mimic large bowel cancer in humans or the gastrointestinal inflammation which frequently precedes it. Dextran sodium sulphate (DSS)-induces colitis in many animal models and has been used in combination with the carcinogen azoxymethane (AOM) to induce cancer in mice. Smad3(-/-) mice are deficient in the transforming growth factor beta (TGFβ) signaling molecule, SMAD3, resulting in dysregulation of the cellular pathway most commonly affected in human colorectal cancer, and develop inflammation-associated colon cancer. Previous studies have shown a requirement for a bacterial trigger for the colitis and colon cancer phenotype in Smad3(-/-) mice. Studies presented here in Smad3(-/-) mice detail disease induction with DSS, without the use of AOM, and show a) Smad3(-/-) mice develop a spectrum of lesions ranging from acute and chronic colitis, crypt herniation, repair, dysplasia, adenomatous polyps, disseminated peritoneal adenomucinosis, adenocarcinoma, mucinous adenocarcinoma (MAC) and squamous metaplasia; b) the colon lesions have variable galactin-3 (Mac2) staining c) increased DSS concentration and duration of exposure leads to increased severity of colonic lesions; d) heterozygosity of SMAD3 does not confer increased susceptibility to DSS-induced disease and e) disease is partially controlled by the presence of T and B cells as Smad3(-/-) Rag2(-/-) double knock out (DKO) mice develop a more severe disease phenotype. DSS-induced disease in Smad3(-/-) mice may be a useful animal model to study not only inflammation-driven MAC but other human diseases such as colitis cystica profunda (CCP) and pseudomyxomatous peritonei (PMP).
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