ArticleMediators of inflammation2022
DNMT3a-Mediated Enterocyte Barrier Dysfunction Contributes to Ulcerative Colitis via Facilitating the Interaction of Enterocytes and B Cells.
Article in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- TNFSF13 insufficiency disrupts human colonic epithelial cell growth and associated B cell dynamics.The Journal of clinical investigation · 2026Article
- Epigenetic Landscapes in Ulcerative Colitis: From Mechanistic Insights to Clinical Translation.ACS omega · 2025Review
- The interaction between gut microbiota and host DNA methylation in the pathogenesis and therapy of inflammatory bowel disease.Frontiers in microbiology · 2025Review
- HMGCS2 and AMACR as potential targets linking mitochondrial dysfunction and ulcerative colitis.Scientific reports · 2024Article
- Altered DNA methylation within DNMT3A, AHRR, LTA/TNF loci mediates the effect of smoking on inflammatory bowel disease.Nature communications · 2024Article
- Ulcerative Colitis Concomitant with Cytomegalovirus Infection, Bullous Sweet's Syndrome, and Acute Myeloid Leukemia: A Case Report and Literature Review.Journal of inflammation research · 2023Article
- Molecular regulation after mucosal injury and regeneration in ulcerative colitis.Frontiers in molecular biosciences · 2022Review
- PFKFB3 Increases IL-1Journal of oncology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Dysfunction of the enterocyte barrier is associated with the development of ulcerative colitis (UC). This study was aimed at exploring the effect of DNMT3a on enterocyte barrier function in the progression of UC and the underlying mechanism. Method: Mice were given 3.5% dextran sodium sulphate (DSS) in drinking water to induce colitis. The primary intestinal epithelial cells (IECs) were isolated and treated with lipopolysaccharide (LPS) to establish an Result: DSS treatment significantly reduced the body weight and colonic length, increased disease activity index (DAI), and aggravated histopathological damage. In addition, DSS treatment induced downregulation of tight junction (TJ) protein, anti-inflammatory cytokines (IL-10 and TGF- Conclusion: Our study suggests that DNMT3a induces enterocyte barrier dysfunction to aggravate UC progression via TNFSF13-mediated interaction of enterocyte and B cells.
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Registered trials
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