ArticleScientific reports2016
The arachidonic acid metabolite 11β-ProstaglandinF2α controls intestinal epithelial healing: deficiency in patients with Crohn's disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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.
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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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Global research status and trends of enteric glia: a bibliometric analysis.Frontiers in pharmacology · 2024Pooled it
- Oral Recombinant Human Collagen III Protects Gastric Mucosa via G-Quadruplex-Mediated Activation of the Pla2g4a-Prostaglandin Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Differentiating Enteric Glial Cells Within Intestinal Organoids Derived from Human Pluripotent Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Article
- The Physiology of Enteric Glia.Annual review of physiology · 2025Review
- Enteric glial cell network function is required for epithelial barrier restitution following intestinal ischemic injury in the early postnatal period.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- From the Gut to the Brain: The Role of Enteric Glial Cells and Their Involvement in the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2024Review
- Mini-Review: Enteric glia of the tumor microenvironment: An affair of corruption.Neuroscience letters · 2023Review
- Mini-Review: Enteric glial regulation of the gastrointestinal epithelium.Neuroscience letters · 2023Review
- Crosstalk between omega-6 oxylipins and the enteric nervous system: Implications for gut disorders?Frontiers in medicine · 2023Review
- Opioid Use, Gut Dysbiosis, Inflammation, and the Nervous System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Review
- Synbiotic Compositions ofNutrients · 2022Article
- Schwann Cells in Digestive System Disorders.Cells · 2022Review
- Maternal prebiotic supplementation impacts colitis development in offspring mice.Frontiers in nutrition · 2022Article
- Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases.International journal of molecular sciences · 2021Review
- Enteric glial biology, intercellular signalling and roles in gastrointestinal disease.Nature reviews. Gastroenterology & hepatology · 2021Review
- Nutraceuticals and Enteric Glial Cells.Molecules (Basel, Switzerland) · 2021Review
- Maternal dietary omega-3 deficiency worsens the deleterious effects of prenatal inflammation on the gut-brain axis in the offspring across lifetime.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Tumor cells hijack enteric glia to activate colon cancer stem cells and stimulate tumorigenesis.EBioMedicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In healthy gut enteric glial cells (EGC) are essential to intestinal epithelial barrier (IEB) functions. In Crohn's Disease (CD), both EGC phenotype and IEB functions are altered, but putative involvement of EGC in CD pathogenesis remains unknown and study of human EGC are lacking. EGC isolated from CD and control patients showed similar expression of glial markers and EGC-derived soluble factors (IL6, TGF-β, proEGF, GSH) but CD EGC failed to increase IEB resistance and healing. Lipid profiling showed that CD EGC produced decreased amounts of 15-HETE, 18-HEPE, 15dPGJ2 and 11βPGF2α as compared to healthy EGC. They also had reduced expression of the L-PGDS and AKR1C3 enzymes. Produced by healthy EGC, the 11βPGF2 activated PPARγ receptor of intestinal epithelial cells to induce cell spreading and IEB wound repair. In addition to this novel healing mechanism our data show that CD EGC presented impaired ability to promote IEB functions through defect in L-PGDS-AKR1C3-11βPGF2α dependent pathway.
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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.