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Moreover, the expression of AQP1 was significantly increased in the CAV1 KO mice (PTemsirolimus research buy transduction. Consequently, AQP1 and CAV1 might be closely associated, and may play a role in bladder dysfunction. To the best of our knowledge, this is the first in vivo study that demonstrates the possible manifestation of AQP1/CAV1-mediated suburothelial cell signaling MRIP in bladder dysfunction. Various studies have implicated that the urothelium can mediate solute and water transport under specific circumstances [15,16]. The epithelial sodium channel (ENaC) is well known to be responsible for fluid and salt transport across epithelial cell membranes. Investigations have revealed that ENaC shows significantly greater expression in BOO patients with clinical symptoms of bladder dysfunction than in the controls. Clinically, this correlated with the storage symptom score of the patients [17]. However, studies on the expression of AQPs in the urinary bladder are limited. In our previous report, detrusor overactivity caused by BOO led to a significant increase in the expression of AQP2�C3, and nitric oxide synthase (endothelial PD173074 molecular weight nitric oxide synthase, neuronal nitric oxide synthase) in rat urinary bladder. In the study, we suggested that the AQPs and nitric oxide synthase isoforms might have a specific role in bladder dysfunction that is related with bladder change following BOO [12]. The CAV1 KO mouse has been proposed as a novel animal model to study bladder impairment associated with primary hypocontraction of urinary bladder and detrusor overactivity [11,18]. Studies on CAV1 KO mice have established that loss of CAV1 is associated with disrupted muscarinic cholinergic activity. This induces impaired smooth muscle contraction in the urinary bladder upon stimulation with carbachol [19,20]. Further, in the organ bath study using bladder strips of CAV1 KO mice (produced by genetic ablation of caveolae), a 70% decrease in acetylcholine release from bladder nerve terminals was observed [11].