ArticlePloS one2014
Altered detrusor gap junction communications induce storage symptoms in bladder inflammation: a mouse cyclophosphamide-induced model of cystitis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Animal Models of Hunner-Type Interstitial Cystitis.International journal of urology : official journal of the Japanese Urological Association · 2026Review
- Pathophysiology and multi-target prevention strategies for cyclophosphamide-induced bladder injury.iScience · 2026Review
- Wireless electrostimulation implants enable sphincter neuromuscular improvement toward mixed urinary incontinence.Nature communications · 2026Article
- Intravesical Instillation with Vivo-Morpholino Nerve Growth Factor Antisense Therapy Ameliorates Acute Interstitial Cystitis/Painful Bladder Syndrome-Related Urinary Frequency in a Rat Model.International urogynecology journal · 2026Article
- SPHK1/S1PR1/PPAR-α axis restores TJs between uroepithelium providing new ideas for IC/BPS treatment.Life science alliance · 2025Article
- Real-Time Void Spot Assay.Journal of visualized experiments : JoVE · 2023Article
- Animal models of interstitial cystitis/bladder pain syndrome.Frontiers in physiology · 2023Review
- Flavonoid Nobiletin Attenuates Cyclophosphamide-Induced Cystitis in Mice through Mechanisms That Involve Inhibition of IL-1β Induced Connexin 43 Upregulation and Gap Junction Communication in Urothelial Cells.International journal of molecular sciences · 2022Article
- Role of detrusor PDGFRαScientific reports · 2022Article
- The Potential of Asiatic Acid in the Reversion of Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats.International journal of molecular sciences · 2021Article
- Urothelium-Specific Deletion of Connexin43 in the Mouse Urinary Bladder Alters Distension-Induced ATP Release and Voiding Behavior.International journal of molecular sciences · 2021Article
- Gene Therapy for Overactive Bladder: A Review of BK-Channel α-Subunit Gene Transfer.Therapeutics and clinical risk management · 2021Review
- BDNF overexpression in the bladder induces neuronal changes to mediate bladder overactivity.American journal of physiology. Renal physiology · 2018Article
- Hyperpolarization-Activated Cyclic Nucleotide-Gated Non-selective (HCN) Ion Channels Regulate Human and Murine Urinary Bladder Contractility.Frontiers in physiology · 2018Article
- Modulation of Bladder Wall Micromotions Alters Intravesical Pressure Activity in the Isolated Bladder.Frontiers in physiology · 2018Article
- Carbenoxolone inhibits TRPV4 channel-initiated oxidative urothelial injury and ameliorates cyclophosphamide-induced bladder dysfunction.Journal of cellular and molecular medicine · 2017Article
- Fiber type-specific afferent nerve activity induced by transient contractions of rat bladder smooth muscle in pathological states.PloS one · 2017Article
- Proliferation of Interstitial Cells in the Cyclophosphamide-Induced Cystitis and the Preventive Effect of Imatinib.BioMed research international · 2017Article
- A Feasibility Study to Determine Whether Clinical Contrast Enhanced Magnetic Resonance Imaging can Detect Increased Bladder Permeability in Patients with Interstitial Cystitis.The Journal of urology · 2016Article
- AMPK Suppresses Connexin43 Expression in the Bladder and Ameliorates Voiding Dysfunction in Cyclophosphamide-induced Mouse Cystitis.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lower urinary tract symptoms (LUTS) include storage, voiding and post-micturition symptoms, featuring many urological diseases. Storage symptoms are the most frequent among these and associated with overactive bladder and non-bacterial bladder inflammation such as interstitial cystitis/bladder pain syndrome (IC/BPS). Gap junction, a key regulator of hyperactive conditions in the bladder, has been reported to be involved in pathological bladder inflammation. Here we report involvement of gap junction in the etiology of storage symptoms in bladder inflammation. In this study, cyclophosphamide-induced cystitis was adapted as a model of bladder inflammation. Cyclophosphamide-treated mice showed typical storage symptoms including increased urinary frequency and reduced bladder capacity, with concurrent up-regulation of connexin 43 (GJA1), one of the major gap junction proteins in the bladder. In isometric tension study, bladder smooth muscle strips taken from the treated mice showed more pronounced spontaneous contraction than controls, which was attenuated by carbenoxolone, a gap junction inhibitor. In voiding behavior studies, the storage symptoms in the treated mice characterized by frequent voiding were alleviated by 18α-glycyrrhetinic acid, another gap junction inhibitor. These results demonstrate that cyclophosphamide-induced mouse model of cystitis shows clinical storage symptoms related with bladder inflammation and that gap junction in the bladder may be a key molecule of these storage symptoms. Therefore, gap junction in the bladder might be an alternative therapeutic target for storage symptoms in bladder inflammation.
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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.