ArticleMediators of inflammation2014
Synergistic effect of vaginal trauma and ovariectomy in a murine model of stress urinary incontinence: upregulation of urethral nitric oxide synthases and estrogen receptors.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Molecular Processes in Stress Urinary Incontinence: A Systematic Review of Human and Animal Studies.International journal of molecular sciences · 2022Pooled it
- Estradiol Ameliorates Postmenopausal Bladder Dysfunction by Restoring Mitophagy via the miRNA-200/KLF4/mTOR Signaling Pathway.International journal of molecular sciences · 2026Article
- Regenerative Medicine Approaches to Stress Urinary Incontinence.Biomimetics (Basel, Switzerland) · 2026Review
- Regenerative Effect of Vaginal Injections of Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes in Ovariectomized Rats.Aesthetic plastic surgery · 2026Article
- Urethral injection of dedifferentiated fat cells ameliorates sphincter damage and voiding dysfunction in a rat model of persistence stress urinary incontinence.International urology and nephrology · 2022Article
- Review
- Potential therapeutic role of punicalagin against mechanical-trauma-induced stress urinary incontinence via upregulation of Nrf2 and TGF-β1 signaling : Effect of punicalagin on mechanical trauma induced SUI.International urogynecology journal · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms underlying stress urinary incontinence (SUI) are unclear. We aimed to evaluate the molecular alterations in mice urethras following vaginal trauma and ovariectomy (OVX). Twenty-four virgin female mice were equally distributed into four groups: noninstrumented control; vaginal distension (VD) group; OVX group; and VD + OVX group. Changes in leak point pressures (LPPs), genital tract morphology, body weight gain, plasma 17β-estradiol level and expressions of neuronal nitric oxide synthase (nNOS), induced nitric oxide synthase (iNOS), and estrogen receptors (ERs-ERα and ERβ) were analyzed. Three weeks after VD, the four groups differed significantly in genital size and body weight gain. Compared with the control group, the plasma estradiol levels were significantly decreased in the OVX and VD + OVX groups, and LPPs were significantly decreased in all three groups. nNOS, iNOS, and ERα expressions in the urethra were significantly increased in the VD and VD + OVX groups, whereas ERβ expression was significantly increased only in the VD + OVX group. These results show that SUI following vaginal trauma and OVX involves urethral upregulations of nNOS, iNOS, and ERs, suggesting that NO- and ER-mediated signaling might play a role in the synergistic effect of birth trauma and OVX-related SUI pathogenesis.
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