ArticleInvestigative and clinical urology2026
Upregulation of aquaporin-2 and caveolins in rat bladder with outlet obstruction-induced detrusor overactivity.
Article in Investigative and clinical urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeBladder outlet obstruction (BOO) leads to detrusor overactivity (DO) and structural remodeling of the bladder. However, the molecular mechanisms underlying this process remain incompletely understood. MATERIALS AND
methodsIn a rat model of partial BOO, we assessed bladder function via cystometry and evaluated histological changes using hematoxylin and eosin staining. The expression and localization of aquaporin (AQP)-2 and caveolin (CAV)-1, -2, and -3 were analyzed by Western blotting and immunofluorescence in bladder tissues. Additionally, immunostaining was performed in cultured human bladder smooth muscle cells to assess protein co-localization.
resultsBOO rats exhibited elevated detrusor contraction pressure and shortened intercontraction intervals. Histologically, hypertrophied smooth muscle bundles and increased extracellular matrix were observed. Western blot analysis revealed significant upregulation of AQP2 and CAV1-3 in BOO bladders. Tissue immunofluorescence demonstrated increased expression and redistribution of these proteins in the detrusor muscle. Cultured cell analysis confirmed subcellular co-localization of AQP2 with CAV1-3.
conclusionsDO induced by BOO is associated with upregulated expression of AQP2 and CAV1-3 in the urinary bladder. The coexpression observed in bladder cells suggests potential molecular interactions between AQP2 and CAVs that may contribute to the pathophysiology of BOO-related bladder dysfunction.
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