ArticleScientific reports2016
BDNF contributes to IBS-like colonic hypersensitivity via activating the enteroglia-nerve unit.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 45 papers.
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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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Who cites it
45 citing papers in PubMed, 73 citations in OpenAlex.
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- PDE4 inhibitor apremilast ameliorates TNBS-induced irritable bowel syndrome in mice by activating the Nrf-2 signaling pathway in enteric glial cells.Acta pharmacologica Sinica · 2026Article
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- Synergistic Modulation of the Gut-Brain-Immune Axis by a DualJournal of microbiology and biotechnology · 2025Article
- NMDAR2B/PKA/CREB signaling pathway contributes to esophageal neuropathic pain in gastroesophageal reflux disease.World journal of gastroenterology · 2025Article
- Genetic Variations in TrkB.T1 Isoform and Their Association With Somatic and Psychological Symptoms in Individuals With IBS.The journal of pain · 2024Article
- The Stressed Gut: Region-specific Immune and Neuroplasticity Changes in Response to Chronic Psychosocial Stress.Journal of neurogastroenterology and motility · 2023Article
- Article
- The efficacy and neural mechanism of acupuncture therapy in the treatment of visceral hypersensitivity in irritable bowel syndrome.Frontiers in neuroscience · 2023Review
- The Enteric Glia and Its Modulation by the Endocannabinoid System, a New Target for Cannabinoid-Based Nutraceuticals?Molecules (Basel, Switzerland) · 2022Review
- Effect of Reactive EGCs on Intestinal Motility and Enteric Neurons During Endotoxemia.Journal of molecular neuroscience : MN · 2022Article
- Obligatory Activation of SRC and JNK by GDNF for Survival and Axonal Outgrowth of Postnatal Intestinal Neurons.Cellular and molecular neurobiology · 2022Article
- The Ketogenic Diet Improves Gut-Brain Axis in a Rat Model of Irritable Bowel Syndrome: Impact on 5-HT and BDNF Systems.International journal of molecular sciences · 2022Article
- Maintenance of Intestinal Homeostasis in Diarrhea-Predominant Irritable Bowel Syndrome by Electroacupuncture Through Submucosal Enteric Glial Cell-Derived S-Nitrosoglutathione.Frontiers in physiology · 2022Article
- Electroacupuncture Alleviates Visceral Hypersensitivity in IBS-D Rats by Inhibiting EGCs Activity through Regulating BDNF/TrkB Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Progress on the Mechanism of Visceral Hypersensitivity in Nonerosive Reflux Disease.Gastroenterology research and practice · 2022Review
- Role of Enteric Glia as Bridging Element between Gut Inflammation and Visceral Pain Consolidation during Acute Colitis in Rats.Biomedicines · 2021Article
- Growth faltering regardless of chronic diarrhea is associated with mucosal immune dysfunction and microbial dysbiosis in the gut lumen.Mucosal immunology · 2021Article
- Enteric glial biology, intercellular signalling and roles in gastrointestinal disease.Nature reviews. Gastroenterology & hepatology · 2021Review
- Nutraceuticals and Enteric Glial Cells.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The over-expressed colonic brain-derived neurotrophic factor (BDNF) has been reported to be associated with abdominal pain in patients with irritable bowel syndrome (IBS). However, the neuropathological mechanism is unclear. We here investigated the involvement of enteroglial cells (EGCs) and enteric nerves in IBS-like visceral hypersensitivity. We showed that glial fibrillary acidic protein (GFAP), tyrosine receptor kinase B (TrkB) and substance P (SP) were significantly increased in the colonic mucosa of IBS patients. The upregulation of those proteins was also observed in the colon of mice with visceral hypersensitivity, but not in the colon of BDNF(+/-) mice. Functionally, TrkB or EGC inhibitors, or BDNF knockdown significantly suppressed visceral hypersensitivity in mice. Using the EGC cell line, we found that recombinant human BDNF (r-HuBDNF) could directly activate EGCs via the TrkB-phospholipase Cγ1 pathway, thereby inducing a significant upregulation of SP. Moreover, supernatants from r-HuBDNF-activated EGC culture medium, rather than r-HuBDNF alone, triggered markedly augmented discharges in isolated intestinal mesenteric afferent nerves. r-HuBDNF alone could cause mesenteric afferent mechanical hypersensitivity independently, and this effect was synergistically enhanced by activated EGCs. We conclude that EGC-enteric nerve unit may be involved in IBS-like visceral hypersensitivity, and this process is likely initiated by BDNF-TrkB pathway activation.
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What Socratic 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 Socratic graph.