Understanding of the role of urothelium in regulating bladder function is continuing to evolve.While the urothelium is thought to\nfunction primarily as a barrier for preventing injurious substances and microorganisms from gaining access to bladder stroma and\nupper urinary tract, studies indicate it may also function in cell signaling events relating to voiding function. This review highlights\nurothelial abnormalities in bladder pain syndrome/interstitial cystitis (BPS/IC), feline interstitial cystitis (FIC), and nonneurogenic\nidiopathic overactive bladder (OAB). These bladder conditions are typified by lower urinary tract symptoms including urinary\nfrequency, urgency, urgency incontinence, nocturia, and bladder discomfort or pain. Urothelial tissues and cells from affected\nclinical subjects and asymptomatic controls have been compared for expression of proteins and mRNA. Animal models have also\nbeen used to probe urothelial responses to injuries of the urothelium, urethra, or central nervous system, and transgenic techniques\nare being used to test specific urothelial abnormalities on bladder function. BPS/IC, FIC, and OAB appear to share some common\npathophysiology including increased purinergic, TRPV1, andmuscarinic signaling, increased urothelial permeability, and aberrant\nurothelial differentiation. One challenge is to determinewhich of several abnormally regulated signaling pathways is most important\nformediating bladder dysfunction in these syndromes,with a goal of treating these conditions by targeting specific pathophysiology.
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