ArticlePloS one2015
Urinary Bladder Dysfunction in Transgenic Sickle Cell Disease Mice.
Article in PloS one, 2015. 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, 16 citations in OpenAlex.
- Heme Modulates Bladder Contractility Through the HO-CO-sGC-cGMP Pathway: Insights into Sickle Cell Disease-Associated Bladder Dysfunction.Antioxidants (Basel, Switzerland) · 2025Article
- Bladder Dysfunction in Sickle Cell Disease Is Associated with Inflammation and Oxidative Stress.International journal of molecular sciences · 2025Article
- Nocturia and obstructive sleep apnoea.Nature reviews. Urology · 2024Review
- Impact of intravascular hemolysis on functional and molecular alterations in the urinary bladder: implications for an overactive bladder in sickle cell disease.Frontiers in physiology · 2024Article
- Enuresis and overactive bladder in sickle cell patients: a narrative review of the literature.World journal of urology · 2023Review
- Reporting animal research: Explanation and elaboration for the ARRIVE guidelines 2.0.PLoS biology · 2020Article
- Urethral dysfunction in a rat model of chemically induced prostatic inflammation: potential involvement of the MRP5 pump.American journal of physiology. Renal physiology · 2020Article
- Urinary dysfunction in transgenic sickle cell mice: model of idiopathic overactive bladder syndrome.American journal of physiology. Renal physiology · 2019Article
- Hydrophobic bile acids relax rat detrusor contraction via inhibiting the opening of the Na⁺/Ca²⁺ exchanger.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUrological complications associated with sickle cell disease (SCD), include nocturia, enuresis, urinary infections and urinary incontinence. However, scientific evidence to ascertain the underlying cause of the lower urinary tract symptoms in SCD is lacking.
objectiveThus, the aim of this study was to evaluate urinary function, in vivo and ex vivo, in the Berkeley SCD murine model (SS).
methodsUrine output was measured in metabolic cage for both wild type and SS mice (25-30 g). Bladder strips and urethra rings were dissected free and mounted in organ baths. In isolated detrusor smooth muscle (DSM), relaxant response to mirabegron and isoproterenol (1nM-10μM) and contractile response to (carbachol (CCh; 1 nM-100μM), KCl (1 mM-300mM), CaCl2 (1μM-100mM), α,β-methylene ATP (1, 3 and 10 μM) and electrical field stimulation (EFS; 1-32 Hz) were measured. Phenylephrine (Phe; 10nM-100μM) was used to evaluate the contraction mechanism in the urethra rings. Cystometry and histomorphometry were also performed in the urinary bladder.
resultsSS mice present a reduced urine output and incapacity to produce typical bladder contractions and bladder emptying (ex vivo), compared to control animals. In DSM, relaxation in response to a selective β3-adrenergic agonist (mirabegron) and to a non-selective β-adrenergic (isoproterenol) agonist were lower in SS mice. Additionally, carbachol, α, β-methylene ATP, KCl, extracellular Ca2+ and electrical-field stimulation promoted smaller bladder contractions in SS group. Urethra contraction induced by phenylephrine was markedly reduced in SS mice. Histological analyses of SS mice bladder revealed severe structural abnormalities, such as reductions in detrusor thickness and bladder volume, and cell infiltration.
conclusionsTaken together, our data demonstrate, for the first time, that SS mice display features of urinary bladder dysfunction, leading to impairment in urinary continence, which may have an important role in the pathogenesis of the enuresis and infections observed the SCD patients.
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