ArticleInflammatory bowel diseases2013
Chloride channel ClC-2 is a key factor in the development of DSS-induced murine colitis.
Article in Inflammatory bowel diseases, 2013. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
21 citing papers in PubMed, 33 citations in OpenAlex.
- Intestinal Epithelial Tight Junction Barrier Regulation by Novel Pathways.Inflammatory bowel diseases · 2025Review
- Establishment of anMethodsX · 2024Article
- Alpha-tocopherylquinone-mediated activation of the Aryl Hydrocarbon Receptor regulates the production of inflammation-inducing cytokines and ameliorates intestinal inflammation.Mucosal immunology · 2023Article
- Alpha-tocopherylquinone differentially modulates claudins to enhance intestinal epithelial tight junction barrier via AhR and Nrf2 pathways.Cell reports · 2023Article
- Long-Term Use of Proton Pump Inhibitors Disrupts Intestinal Tight Junction Barrier and Exaggerates Experimental Colitis.Journal of Crohn's & colitis · 2023Article
- The ClC-2 Chloride Channel Activator, Lubiprostone, Improves Intestinal Barrier Function in Biopsies from Crohn's Disease but Not Ulcerative Colitis Patients.Pharmaceutics · 2023Article
- Pathophysiological role of ion channels and transporters in gastrointestinal mucosal diseases.Cellular and molecular life sciences : CMLS · 2021Review
- Matrix Metalloproteinase MMP-12 Promotes Macrophage Transmigration Across Intestinal Epithelial Tight Junctions and Increases Severity of Experimental Colitis.Journal of Crohn's & colitis · 2021Article
- Endocytosis of Intestinal Tight Junction Proteins: In Time and Space.Inflammatory bowel diseases · 2021Review
- Mechanism underlying the significant role of the miR-4262/SIRT1 axis in children with inflammatory bowel disease.Experimental and therapeutic medicine · 2020Article
- The Integral Role of Tight Junction Proteins in the Repair of Injured Intestinal Epithelium.International journal of molecular sciences · 2020Review
- E-cadherin Beyond Structure: A Signaling Hub in Colon Homeostasis and Disease.International journal of molecular sciences · 2019Review
- Intestinal epithelial tight junction barrier regulation by autophagy-related protein ATG6/beclin 1.American journal of physiology. Cell physiology · 2019Article
- Knockout of ClC-2 reveals critical functions of adherens junctions in colonic homeostasis and tumorigenicity.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Adiponectin administration alleviates DSS-induced colonic inflammation in Caco-2 cells and mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Genistein improves inflammatory response and colonic function through NF-κB signal in DSS-induced colonic injury.Oncotarget · 2017Article
- Chloride channel ClC- 2 enhances intestinal epithelial tight junction barrier function via regulation of caveolin-1 and caveolar trafficking of occludin.Experimental cell research · 2017Article
- Matrine alleviates lipopolysaccharide-induced intestinal inflammation and oxidative stress via CCR7 signal.Oncotarget · 2017Article
- Hydrogen sulfide from a NaHS source attenuates dextran sulfate sodium (DSS)-induced inflammation via inhibiting nuclear factor-κB.Journal of Zhejiang University. Science. B · 2016Article
- Matrix metalloproteinase 9-induced increase in intestinal epithelial tight junction permeability contributes to the severity of experimental DSS colitis.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPreviously, it was shown that the chloride channel ClC-2 modulates intestinal tight junction (TJ) barrier function. The aim of the present study was to investigate the role of ClC-2 in epithelial barrier function and recovery in the event of epithelial injury.
methodsThe role of ClC-2 was investigated in TJ barrier function in dextran sodium sulfate (DSS)-induced colitis in ClC-2 knockout mice and ClC-2 knockdown intestinal Caco-2 cells. Barrier function was measured electrophysiologically and by transepithelial mannitol fluxes. Selected TJ and associated proteins were Western blotted, cytokines were measured using quantitative PCR, and human colonic biopsies were examined with immunohistochemistry.
resultsClC-2 mice had a higher disease activity index, higher histological scores, and increased paracellular permeability compared with wild-type mice when treated with DSS. DSS-treated ClC-2 mice had increased claudin-2 expression, greater loss of occludin in the membrane, increased association of occludin with caveolin-1, and significantly increased tumor necrosis factor-α and interleukin-1β messenger RNA. ClC-2 knockdown in human intestinal Caco-2 cells resulted in a greater loss of epithelial resistance in the event of epithelial injury. The restoration of colonic barrier function after DSS colitis was delayed in ClC-2 mice. In human colonic biopsies, the protein and messenger RNA expression of ClC-2 was found to be reduced in patients with ulcerative colitis.
conclusionsClC-2 plays a critical role in experimental colitis in that its absence increases disease activity, reduces barrier function and recovery, and perturbs TJs. Furthermore, ClC-2 expression is markedly reduced in the colon of human patients with ulcerative colitis.
Indexed as
Identifiers
What OpenQuestion holds
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.