Hypertrophy occurs in urinary bladder wall smooth muscle (BSM) in men with partial bladder outlet obstruction (PBOO) caused by benign prostatic hyperplasia (BPH) and in animal models of PBOO. Hypertrophied BSM from the rabbit model exhibits downregulation of caveolin-1, a structural and functional protein of caveolae that function as signaling platforms to mediate interaction between receptor proteins and adaptor and effector molecules to regulate signal generation, amplification, and diversification. Caveolin-1 expression is diminished in PBOO-induced BSM hypertrophy in mice and in men with BPH. The proximal promoter of the human and mouse caveolin-1 (CAV1) gene was characterized, and it was observed that the transcription factor GATA-6 binds this promoter, causing reduced expression of caveolin-1. Furthermore, caveolin-1 expression levels inversely correlate with the abundance of GATA-6 in BSM hypertrophy in mice and human beings. Benign prostatic hyperplasia (BPH) is common in aging men and is often associated with lower urinary tract symptoms. Partial bladder outlet obstruction (PBOO) has long been considered a key factor in the mechanism through which BPH causes lower urinary tract symptoms. PBOO-induced lower urinary tract symptoms are associated with bladder wall smooth muscle (BSM) remodeling including hypertrophy, thereby altering bladder contractility.

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