ArticleMolecular neurobiology2014
GDNF is involved in the barrier-inducing effect of enteric glial cells on intestinal epithelial cells under acute ischemia reperfusion stimulation.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 79 citations in OpenAlex.
- Short-Chain Fatty Acids Elicit Differential Expression of Growth Factors and Pro-Inflammatory Cytokines in Immortalized Rat Enteric Glial Cells.Nutrients · 2026Article
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Article
- Glial cell line derived neurotrophic factor (GDNF) induces mucosal healing via intestinal stem cell niche activation.Cell proliferation · 2025Article
- Exploring the diversity of biological processes regulated by glial cell line-derived neurotrophic factor, a pleiotropic molecule with therapeutic potential.Frontiers in physiology · 2025Review
- Article
- 1,25(OH)2D3 supplementation alleviates gut-vascular barrier disruption via inhibition of S100B/ADAM10 pathway.Tissue barriers · 2024Article
- Astrocytes in functional recovery following central nervous system injuries.The Journal of physiology · 2024Review
- Review
- 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
- Potential roles of enteric glial cells in Crohn's disease: A critical review.Cell proliferation · 2024Review
- CORM-3 alleviates the intestinal injury in a rodent model of hemorrhage shock and resuscitation: roles of GFAP-positive glia.Journal of molecular histology · 2023Article
- Mini-Review: Enteric glial regulation of the gastrointestinal epithelium.Neuroscience letters · 2023Review
- Adenosine 2A receptor contributes to the facilitation of post-infectious irritable bowel syndrome by γδ T cellsWorld journal of gastroenterology · 2023Article
- Guardians of the gut: influence of the enteric nervous system on the intestinal epithelial barrier.Frontiers in medicine · 2023Review
- Effect of Reactive EGCs on Intestinal Motility and Enteric Neurons During Endotoxemia.Journal of molecular neuroscience : MN · 2022Article
- Opioid Use, Gut Dysbiosis, Inflammation, and the Nervous System.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Review
- Dexmedetomidine reduces enteric glial cell injury induced by intestinal ischaemia-reperfusion injury through mitochondrial localization of TERT.Journal of cellular and molecular medicine · 2022Article
- Neuroinflammation as an etiological trigger for depression comorbid with inflammatory bowel disease.Journal of neuroinflammation · 2022Review
- Overexpression of microRNA-211 in Functional Dyspepsia via Downregulation of the Glial Cell Line-Derived Neurotrophic Factor (GDNF) by Increasing Phosphorylation of p38 MAPK Pathway.Canadian journal of gastroenterology & hepatology · 2022Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute intestinal ischemia reperfusion (IR) injury is often associated with intestinal epithelial barrier (IEB) dysfunction. Enteric glial cells (EGCs) play an essential role in maintaining the integrity of IEB functions. However, the precise mechanism of EGCs under IR stimulation remains unclear. Here, we report that EGCs are closely involved in the modulation of IEB functions in response to IR challenge. The intestinal IR treatment led to the significant upregulation of the EGC activation marker, glial fibrillary acidic protein, accompanied by the increasing abundance of glial-derived neurotrophic factor (GDNF) and inducible nitric oxidase (iNOS) proteins, which was also confirmed in in vitro hypoxia reoxygenation (HR) tests. Co-culturing with EGCs attenuated the tight junctional abnormalities, blocked the downregulation of ZO-1 and occludin protein expression, and relieved the decrease of permeability of intestinal epithelial cell (IEC) monolayers under HR treatment. Furthermore, exogenous GDNF administration displays the barrier-protective effects similar to EGCs against HR stimulation, while RNA interference-mediated knockdown of GDNF significantly inhibited the protective capability of EGCs. The expression of both GDNF and iNOS proteins of EGCs was significantly upregulated by co-culturing with IECs, which was further increased by HR treatment. Interestingly, through inhibiting iNOS activity, the barrier-protective effect of EGCs was influenced in normal condition but enhanced in HR condition. These results suggest that GDNF plays an important role in the barrier-protective mechanism of activated EGCs under IR stimulation, whereas EGCs (via iNOS release) are also involved in intestinal inflammation response, which may contribute to IEB damage induced by IR injury.
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