ArticleThe Journal of clinical investigation2019
Neurotrophic factor GDNF regulates intestinal barrier function in inflammatory bowel disease.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 104 citations in OpenAlex.
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- Short-Chain Fatty Acids Elicit Differential Expression of Growth Factors and Pro-Inflammatory Cytokines in Immortalized Rat Enteric Glial Cells.Nutrients · 2026Article
- Molecular links between inflammatory bowel disease and Alzheimer's disease through immune signaling and inflammatory pathways.World journal of gastroenterology · 2025Review
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Inhibition of GDNF-Driven Macrophage-to-Myofibroblast Transition Protects Against Colitis-Associated Intestinal Fibrosis.Inflammation · 2025Article
- The Impact of Endocrine Disruptors on the Female Genital Tract Microbiome: A Narrative Review.Life (Basel, Switzerland) · 2025Review
- Promoting mucosal healing by targeting TMEM219-dependent intestinal epithelial stem cell defects in inflammatory bowel disease.The Journal of clinical investigation · 2025Article
- Assembly of MSCs into a spheroid configuration increases poly(I:C)-mediated TLR3 activation and the immunomodulatory potential of MSCs for alleviating murine colitis.Stem cell research & therapy · 2025Article
- Glial cell line-derived neurotrophic factor improves impaired colonic motility in experimental colitis mice through connexin 43.World journal of gastroenterology · 2025Article
- Glial cell line derived neurotrophic factor (GDNF) induces mucosal healing via intestinal stem cell niche activation.Cell proliferation · 2025Article
- Glial cell line-derived neurotrophic factor inhibits mast-cell-like RBL-2H3 cells activation via Ca2+-mediated degranulation and Ca2+/CaMKⅡ/JNK pathway.Frontiers in pharmacology · 2025Article
- Endosomal Trafficking Bypassed by the RAB5B-CD109 Interplay Promotes Axonogenesis in KRAS-Mutant Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Impact of Pentraxin 3 on Crohn's Disease Phenotype.International journal of molecular sciences · 2024Article
- A living organoid biobank of patients with Crohn's disease reveals molecular subtypes for personalized therapeutics.Cell reports. Medicine · 2024Article
- GDNF's Role in Mitigating Intestinal Reactive Gliosis and Inflammation to Improve Constipation and Depressive Behavior in Rats with Parkinson's disease.Journal of molecular neuroscience : MN · 2024Article
- Article
- In Vitro Models for Investigating Intestinal Host-Pathogen Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Potential roles of enteric glial cells in Crohn's disease: A critical review.Cell proliferation · 2024Review
- The impact of signaling pathways on the desmosome ultrastructure in pemphigus.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired intestinal epithelial barrier (IEB) function with loss of desmosomal junctional protein desmoglein 2 (DSG2) is a hallmark in the pathogenesis of inflammatory bowel disease (IBD). While previous studies have reported that glial cell line-derived neurotrophic factor (GDNF) promotes IEB function, the mechanisms are poorly understood. We hypothesized that GDNF is involved in the loss of DSG2, resulting in impaired IEB function as seen in IBD. In the inflamed intestine of patients with IBD, there was a decrease in GDNF concentrations accompanied by a loss of DSG2, changes of the intermediate filament system, and increased phosphorylation of p38 MAPK and cytokeratins. DSG2-deficient and RET-deficient Caco2 cells revealed that GDNF specifically recruits DSG2 to the cell borders, resulting in increased DSG2-mediated intercellular adhesion via the RET receptor. Challenge of Caco2 cells and enteroids with proinflammatory cytokines as well as dextran sulfate sodium-induced (DSS-induced) colitis in C57Bl/6 mice led to impaired IEB function with reduced DSG2 mediated by p38 MAPK-dependent phosphorylation of cytokeratins. GDNF blocked all inflammation-induced changes in the IEB. GDNF attenuates inflammation-induced impairment of IEB function caused by the loss of DSG2 through p38 MAPK-dependent phosphorylation of cytokeratin. The reduced GDNF in patients with IBD indicates a disease-relevant contribution to the development of IEB dysfunction.
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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.