ArticleThe Journal of clinical investigation1999
A paradoxical reduction in susceptibility to colonic injury upon targeted transgenic ablation of goblet cells.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 61 citations in OpenAlex.
- Pathobiont-triggered induction of goblet cell response drives regional susceptibility to inflammatory bowel disease.The Journal of clinical investigation · 2026Article
- Article
- From Crypts to Cancer: A Holistic Perspective on Colorectal Carcinogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease.Journal of neuroinflammation · 2022Review
- Cadmium ingestion exacerbates Salmonella infection, with a loss of goblet cells through activation of Notch signaling pathways by ROS in the intestine.Journal of hazardous materials · 2020Article
- Mechanisms of Disease: Inflammatory Bowel Diseases.Mayo Clinic proceedings · 2019Review
- Review
- Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Nexus Implicated in Bowel Disease Pathophysiology.International journal of molecular sciences · 2017Review
- The Endoplasmic Reticulum Stress Sensor IRE1α in Intestinal Epithelial Cells Is Essential for Protecting against Colitis.The Journal of biological chemistry · 2015Article
- Article
- Guanylate cyclase C deficiency causes severe inflammation in a murine model of spontaneous colitis.PloS one · 2013Article
- Actin reorganization as the molecular basis for the regulation of apoptosis in gastrointestinal epithelial cells.Cell death and differentiation · 2012Article
- Murine guanylate cyclase C regulates colonic injury and inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Altered intestinal epithelial homeostasis in mice with intestine-specific deletion of the Krüppel-like factor 4 gene.Developmental biology · 2011Article
- Early-stage blocking of Notch signaling inhibits the depletion of goblet cells in dextran sodium sulfate-induced colitis in mice.Journal of gastroenterology · 2010Article
- Disruption of Paneth and goblet cell homeostasis and increased endoplasmic reticulum stress in Agr2-/- mice.Developmental biology · 2010Article
- Endoplasmic reticulum stress and intestinal inflammation.Mucosal immunology · 2010Review
- Colitis-associated variant of TLR2 causes impaired mucosal repair because of TFF3 deficiency.Gastroenterology · 2009Article
- Endoplasmic reticulum stress in the intestinal epithelium and inflammatory bowel disease.Seminars in immunology · 2009Review
- Alteration of ocular surface mucins in MUC5AC-DTA transgenic mice.Molecular vision · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Goblet cells are the major mucus-producing cells of the intestine and are presumed to play an important role in mucosal protection. However, their functional role has not been directly assessed in vivo. In initial studies, a 5' flanking sequence of the murine intestinal trefoil factor (ITF) gene was found to confer goblet cell-specific expression of a transgene. To assess the role of goblet cells in the intestine, we generated transgenic mice in which approximately 60% of goblet cells were ablated by the expression of an attenuated diphtheria toxin (DT) gene driven by the ITF promoter; other cell lineages were unaffected. We administered 2 exogenous agents, dextran sodium sulfate (DSS) and acetic acid, to assess the susceptibility of mITF/DT-A transgenic mice to colonic injury. After oral administration of DSS, 55% of control mice died, whereas DT transgenic mice retained their body weight and less than 5% died. Similarly, 30% of the wild-type mice died after mucosal administration of acetic acid, compared with 3.2% of the transgenic mice. Despite the reduction in goblet-cell number, the total amount of ITF was increased in the mITF/DT-A transgenic mice, indicating inducible compensatory mechanisms. These results suggest that goblet cells contribute to mucosal protection and repair predominantly through production of trefoil peptides.
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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.