ArticleExperimental neurology2010
Experimental colitis triggers the release of substance P and calcitonin gene-related peptide in the urinary bladder via TRPV1 signaling pathways.
Article in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 79 citations in OpenAlex.
- Plant-Derived Spinacetin Mitigates Cyclophosphamide-Induced Hemorrhagic Cystitis in Rats.International journal of molecular sciences · 2026Article
- Exploring the oral bacteria-oral lichen planus connection: mechanisms, clinical implications and future directions.Archives of microbiology · 2025Review
- The Role of TRPV1/CGRP Pathway Activated byInternational journal of molecular sciences · 2025Article
- Therapeutic Approaches for Urologic Chronic Pelvic Pain Syndrome; Management: Research Advances, Experimental Targets, and Future Directions.The Journal of pharmacology and experimental therapeutics · 2024Review
- CGRP Released by Corneal Sensory Nerve Maintains Tear Secretion of the Lacrimal Gland.Investigative ophthalmology & visual science · 2024Article
- Enhancement sensitivity of TRPV1 in dorsal root ganglia via the SP-NK-1 pathway contributes to increased bladder organ sensitivity caused by prostatitis.Frontiers in neuroscience · 2024Article
- Bibliometric analysis of recent research on the association between TRPV1 and inflammation.Channels (Austin, Tex.) · 2023Article
- Hemodynamic and neurobiological factors for the development of chronic pelvic pain in patients with pelvic venous disorder.Journal of vascular surgery. Venous and lymphatic disorders · 2023Article
- Ultrasonographic assessment of skeletal muscles after experimentally induced neurogenic inflammation (facet injury) in rats.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Upregulation of P2X3 receptors in primary afferent pathways involves in colon-to-bladder cross-sensitization in rats.Frontiers in physiology · 2022Article
- Inhibition of CXCR4 in Spinal Cord and DRG with AMD3100 Attenuates Colon-Bladder Cross-Organ Sensitization.Drug design, development and therapy · 2022Article
- Functional segregation within the pelvic nerve of male rats: a meso- and microscopic analysis.Journal of anatomy · 2020Article
- Electroacupuncture intervention of visceral hypersensitivity is involved in PAR-2-activation and CGRP-release in the spinal cord.Scientific reports · 2020Article
- Ubiquitin carboxyl-terminal hydrolase L1 promotes hypoxia-inducible factor 1-dependent tumor cell malignancy in spheroid models.Cancer science · 2020Article
- TRPV1, TRPA1, and TRPM8 are expressed in axon terminals in the cornea: TRPV1 axons contain CGRP and secretogranin II; TRPA1 axons contain secretogranin 3.Molecular vision · 2020Article
- Long-lasting bladder overactivity and bladder afferent hyperexcitability in rats with chemically-induced prostatic inflammation.The Prostate · 2019Article
- Potential Mechanisms Underlying Centralized Pain and Emerging Therapeutic Interventions.Frontiers in cellular neuroscience · 2018Review
- The Expression of Transcription Factors Mecp2 and CREB Is Modulated in Inflammatory Pelvic Pain.Frontiers in systems neuroscience · 2018Article
- Mechanisms Underlying Overactive Bladder and Interstitial Cystitis/Painful Bladder Syndrome.Frontiers in neuroscience · 2018Review
- Genitourinary and gastrointestinal co-morbidities in children: The role of neural circuits in regulation of visceral function.Journal of pediatric urology · 2017Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Clinical data provide evidence of high level of co-morbidity among genitourinary and gastrointestinal disorders characterized by chronic pelvic pain. The objective of this study was to test the hypothesis that colonic inflammation can impact the function of the urinary bladder via activation of TRPV1 signaling pathways followed by alterations in gene and protein expression of substance P (SP) and calcitonin gene-related peptide (CGRP) in sensory neurons and in the bladder. Inflammation was induced by intracolonic instillation of trinitrobenzene sulfonic acid (TNBS, 12.5mg/kg), and desensitization of TRPV1 receptors was evoked by intracolonic resiniferatoxin (RTX, 10(-)(7)M). mRNA and protein concentrations of CGRP and SP were measured at 3, 5 and 30 days. RTX instillation in the colon caused 3-fold up-regulation of SP mRNA in the urinary bladder at day 5 (n=7, p ≤ 0.05) followed by 35-fold increase at day 30 (n=5, p ≤ 0.05). Likewise, TNBS colitis triggered 15.8-fold up-regulation of SP mRNA 1 month after TNBS (n=5, p ≤ 0.05). Desensitization of colonic TRPV1 receptors prior to TNBS abolished SP increase in the urinary bladder. RTX led to 4.3-fold increase of CGRP mRNA at day 5 (n=7, p ≤ 0.05 to control) in the bladder followed by 28-fold increase at day 30 post-RTX (n=4, p ≤ 0.05). Colitis did not alter CGRP concentration during acute phase; however, at day 30 mRNA level was increased by 17.8 ± 6.9-fold (n=5, p ≤ 0.05) in parallel with 4-fold increase in CGRP protein (n=5, p ≤ 0.01) in the detrusor. Protein concentration of CGRP in the spinal cord was diminished by 45-65% (p ≤ 0.05) during colitis. RTX pretreatment did not affect CGRP concentration in the urinary bladder; however, it caused a reduction in CGRP release from lumbosacral DRG neurons during acute phase (3 and 5 days post-TNBS). Our results clearly demonstrate that colonic inflammation triggers the release of pro-inflammatory neuropeptides SP and CGRP in the urinary bladder via activation of TRPV1 signaling mechanisms enunciating the neurogenic nature of pelvic organ cross-sensitization.
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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.