ArticleBritish journal of pharmacology2015
Urinary bladder inflammation induces changes in urothelial nerve growth factor and TRPV1 channels.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Molecular Mechanism Operating in Animal Models of Neurogenic Detrusor Overactivity: A Systematic Review Focusing on Bladder Dysfunction of Neurogenic Origin.International journal of molecular sciences · 2023Pooled it
- Repeated intravesical injections of platelet-rich plasma improve symptoms and alter urinary functional proteins in patients with refractory interstitial cystitis.Scientific reports · 2020Trial
- The association between the systemic inflammation response index and overactive bladder: a cross-sectional study.European journal of medical research · 2025Article
- Role and mechanism of Roux-en-Y gastric bypass in the treatment of diabetic urinary bladder hyperactivity by reducing TRPV1 and P2X3.World journal of diabetes · 2025Article
- Purine nucleoside phosphorylase inhibition is an effective approach for the treatment of chemical hemorrhagic cystitis.JCI insight · 2024Article
- Review
- Peripheral Cannabinoid-1 Receptor Blockade Ameliorates Cystitis Severity.Cannabis and cannabinoid research · 2023Article
- Animal models of interstitial cystitis/bladder pain syndrome.Frontiers in physiology · 2023Review
- Use of Intravesical Injections of Platelet-Rich Plasma for the Treatment of Bladder Pain Syndrome: A Comprehensive Literature Review.Antibiotics (Basel, Switzerland) · 2021Review
- Activation of GPR18 by Resolvin D2 Relieves Pain and Improves Bladder Function in Cyclophosphamide-Induced Cystitis Through Inhibiting TRPV1.Drug design, development and therapy · 2021Article
- The role of prostaglandin and E series prostaglandin receptor type 4 receptors in the development of bladder overactivity in a rat model of chemically induced prostatic inflammation.BJU international · 2019Article
- Partners in Crime: NGF and BDNF in Visceral Dysfunction.Current neuropharmacology · 2019Review
- Modulation of lower urinary tract smooth muscle contraction and relaxation by the urothelium.Naunyn-Schmiedeberg's archives of pharmacology · 2018Review
- Increased Piezo1 channel activity in interstitial Cajal-like cells induces bladder hyperactivity by functionally interacting with NCX1 in rats with cyclophosphamide-induced cystitis.Experimental & molecular medicine · 2018Article
- Disulfide high mobility group box-1 causes bladder pain through bladder Toll-like receptor 4.BMC physiology · 2017Article
- Cyclophosphamide-induced HCN1 channel upregulation in interstitial Cajal-like cells leads to bladder hyperactivity in mice.Experimental & molecular medicine · 2017Article
- Capsaicin, Nociception and Pain.Molecules (Basel, Switzerland) · 2016Review
- Nerve growth factor and diarrhea-predominant irritable bowel syndrome (IBS-D): a potential therapeutic target?Journal of Zhejiang University. Science. B · 2016Review
- Activation of cannabinoid receptor 1 inhibits increased bladder activity induced by nerve growth factor.Neuroscience letters · 2015Article
- Repeated intravesical injections of platelet-rich plasma are safe and effective in the treatment of interstitial cystitis/bladder pain syndrome.Tzu chi medical journalArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
background and purposeThe urinary bladder urothelium expresses various receptors and in response to chemical and mechanical stimuli releases mediators, thereby modulating bladder sensory pathways. Transient receptor potential vanilloid 1 (TRPV1) ion channels and nerve growth factor (NGF) in those cells are implicated in this modulatory effect and play a role in sensitizing pain-related afferent pathways during inflammation. In this study, we investigated the interaction between NGF and TRPV1 channels in urothelial cells. EXPERIMENTAL APPROACH: Urothelial cells from female Sprague-Dawley rat bladders were cultured to quantify membrane expression of TRPV1 channels and capsaicin-induced ATP release in the presence of NGF alone or with TrKA or PI3K inhibitors. Pain scores from rats with cyclophosphamide (CYP)-induced bladder inflammation were assessed after treatment with a TrkA antagonist. Bladders (from control and CYP rats) were collected and analysed for NGF content and TRPV1 channel expression. KEY
resultsCultured cells responded to NGF with increased TRPV1 channel expression in the cell membrane and increased release of ATP. Both responses were blocked by either a TrkA antagonist or a PI3K inhibitor. Treatment in vivo with the TrkA antagonist alleviated pain symptoms and reduced CYP-induced NGF overexpression in the mucosa. Furthermore, in urothelial cells from animals with bladder inflammation, expression of TRPV1 channels in the membrane was significantly increased. CONCLUSIONS AND IMPLICATIONS: During bladder inflammation, increased production of NGF in urothelial cells induced increased expression and activity of TRPV1 channels in the cell membrane. This effect was primarily mediated by the PI3K pathway.
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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.