ArticlePloS one2012
Opposite role of tumor necrosis factor receptors in dextran sulfate sodium-induced colitis in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- ADAM17 and its proteolytic targets in disease pathogenesis.The FEBS journal · 2026Review
- Derivation of novel metabolic pathway score identifies alanine metabolism as a targetable influencer of TNF-alpha signaling.Heliyon · 2024Article
- Involvement of DNA Damage Response via the Ccndbp1-Atm-Chk2 Pathway in Mice with Dextran-Sodium-Sulfate-Induced Colitis.Journal of clinical medicine · 2022Article
- Exfoliated epithelial cell transcriptome reflects both small and large intestinal cell signatures in piglets.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Immunonutritional Bioactives fromNutrients · 2021Article
- LncRNA NEAT1 mediates intestinal inflammation by regulating TNFRSF1B.Annals of translational medicine · 2021Article
- TNF Receptor 1 Promotes Early-Life Immunity and Protects against Colitis in Mice.Cell reports · 2020Article
- Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects.Frontiers in immunology · 2020Review
- The many faces of tumor necrosis factor signaling in the intestinal epithelium.Genes and immunity · 2019Review
- Spliceosome protein Eftud2 promotes colitis-associated tumorigenesis by modulating inflammatory response of macrophage.Mucosal immunology · 2019Article
- Critical Role of Tumor Necrosis Factor Signaling in Mesenchymal Stem Cell-Based Therapy for Autoimmune and Inflammatory Diseases.Frontiers in immunology · 2018Review
- MDSCs are involved in the protumorigenic potentials of GM-CSF in colitis-associated cancer.International journal of immunopathology and pharmacology · 2017Article
- NLRP6 function in inflammatory monocytes reduces susceptibility to chemically induced intestinal injury.Mucosal immunology · 2017Article
- TNFR2 expression by CD4 effector T cells is required to induce full-fledged experimental colitis.Scientific reports · 2016Article
- G2A Signaling Dampens Colitic Inflammation via Production of IFN-γ.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Redeeming an old foe: protective as well as pathophysiological roles for tumor necrosis factor in inflammatory bowel disease.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- A gut microbial metabolite of linoleic acid, 10-hydroxy-cis-12-octadecenoic acid, ameliorates intestinal epithelial barrier impairment partially via GPR40-MEK-ERK pathway.The Journal of biological chemistry · 2015Article
- Neutrophil infiltration favors colitis-associated tumorigenesis by activating the interleukin-1 (IL-1)/IL-6 axis.Mucosal immunology · 2014Article
- TNF blocking therapies and immunomonitoring in patients with inflammatory bowel disease.Mediators of inflammation · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-α (TNF-α) is a key factor for the pathogenesis of inflammatory bowel diseases (IBD), whose function is known to be mediated by TNF receptor 1 (TNFR1) or 2. However, the precise role of the two receptors in IBD remains poorly understood. Herein, acute colitis was induced by dextran sulfate sodium (DSS) instillation in TNFR1 or 2-/- mice. TNFR1 ablation led to exacerbation of signs of colitis, including more weight loss, increased mortality, colon shortening and oedema, severe intestinal damage, and higher levels of myeloperoxidase compared to wild-type counterparts. While, TNFR2 deficiency had opposite effects. This discrepancy was reflected by alteration of proinflammatory cytokine and chemokine production in the colons. Importantly, TNFR1 ablation rendered enhanced apoptosis of colonic epithelial cells and TNFR2 deficiency conferred pro-apoptotic effects of lamina propria (LP)-immune cells, as shown by the decreased ratio of Bcl-2/Bax and enhanced nuclear factor (NF)-κB activity.
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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.