ArticleJournal of molecular neuroscience : MN2016
Effects of CYP-Induced Cystitis on Growth Factors and Associated Receptor Expression in Micturition Pathways in Mice with Chronic Overexpression of NGF in Urothelium.
Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Alpha-Linolenic Acid and Tarantula Cubensis Extract Attenuate Bladder Inflammation in Cyclophosphamide-Induced Cystitis: A Comparative Experimental Study.International urogynecology journal · 2026Article
- The Role of TRPV4 in Repeated Variate Stress-Induced Increases in Voiding Frequency and Somatic Sensitivity in Male and Female Mice.Journal of molecular neuroscience : MN · 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
- Efficacy of bladder instillations with adelmidrol and sodium hyaluronate for the treatment of symptomatic radiation cystitis.Frontiers in surgery · 2025Article
- TrkA inhibition alleviates bladder overactivity in cyclophosphamide-induced cystitis by targeting hyperpolarization-activated cyclic nucleotide-gated channels.Iranian journal of basic medical sciences · 2023Article
- Imatinib Mesylate Reduces Neurotrophic Factors and pERK and pAKT Expression in Urinary Bladder of Female Mice With Cyclophosphamide-Induced Cystitis.Frontiers in systems neuroscience · 2022Article
- The Effect of Chronic Psychological Stress on Lower Urinary Tract Function: An Animal Model Perspective.Frontiers in physiology · 2022Review
- Urine Proteomic Study in OAB Patients-Preliminary Report.Journal of clinical medicine · 2020Article
- Urine: Waste product or biologically active tissue?Neurourology and urodynamics · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have determined if cyclophosphamide (CYP)-induced cystitis produces additional changes in growth factor/receptors expression in the urinary bladder (urothelium, detrusor) and lumbosacral (L6-S1) dorsal root ganglia (DRG) in a transgenic mouse model with chronic urothelial overexpression of NGF (NGF-OE). Functionally, NGF-OE mice treated with CYP exhibit significant increases in voiding frequency above that observed in control NGF-OE mice (no CYP). Quantitative PCR was used to determine NGF, BDNF, VEGF, and receptors (TrkA, TrkB, p75(NTR)) transcripts expression in tissues from NGF-OE and wild-type (WT) mice with CYP-induced cystitis of varying duration (4 h, 48 h, 8 days). In urothelium of control NGF-OE mice, NGF mRNA was significantly (p ≤ 0.001) increased. Urothelial expression of NGF mRNA in NGF-OE mice treated with CYP (4 h, 48 h, 8 days) was not further increased but maintained with all durations of CYP treatment evaluated. In contrast, CYP-induced cystitis (4 h, 48 h, 8 days) in NGF-OE mice demonstrated significant (p ≤ 0.05) regulation in BDNF, VEGF, TrkA, TrkB, and P75(NTR) mRNA in urothelium and detrusor smooth muscle. Similarly, CYP-induced cystitis (4 h, 48 h, 8 days) in NGF-OE mice resulted in significant (p ≤ 0.05), differential changes in transcript expression for NGF, BDNF, and receptors (TrkA, TrkB, p75(NTR)) in S1 DRG that was dependent on the duration-of CYP-induced cystitis. In general, NGF, BDNF, TrkA, and TrkB protein content in the urinary bladder increased in WT and NGF-OE mice with CYP-induced cystitis (4 h). Changes in NGF, TrkA and TrkB expression in the urinary bladder were significantly (p ≤ 0.05) greater in NGF-OE mice with CYP-induced cystitis (4 h) compared to WT mice with cystitis (4 h). However, the magnitude of change between WT and NGF-OE mice was only significantly (p ≤ 0.05) different for TrkB expression in urinary bladder of NGF-OE mice treated with CYP. These studies are consistent with target-derived NGF and other inflammatory mediators affecting neurochemical plasticity with potential contributions to reflex function of micturition pathways.
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