Dados do Trabalho

Título

PIEZO2 is downregulated in the detrusor of men with bladder outlet obstruction and is associated with urinary retention and decreased bladder compliance

Resumo

Introduction: Recent research has highlighted the mechanotransducer PIEZO2 as a crucial factor in lower urinary tract function, associated with bladder compliance, bladder-wall thickening, and elevated bladder pressures.
Goals: This study was an exploratory investigation into the relationship between PIEZO2 expression in the detrusor smooth muscle and lower urinary tract dysfunction. We explored the hypothesis that Piezo2 expression is associated with lower urinary tract dysfunction in men with bladder outlet obstruction due to benign prostatic hyperplasia.
Methods: From September 2014 to January 2016, a consecutive series of patients undergoing open prostatectomy due to benign prostatic hyperplasia at our hospital were included in the study. All participants were submitted to comprehensive preoperative evaluations, including urodynamic assessments. During prostatectomy, a full thickness fragment of the bladder wall was obtained, the mucosa and adventitia were removed and it was later prepared for PIEZO2 mRNA expression analysis. Cadaveric organ donors comprised the control group.
Results: We found that PIEZO2 expression is downregulated in the detrusor of men with benign prostatic hyperplasia when compared to the control group. Among patients with benign prostatic hyperplasia, those in urinary retention with an indwelling catheter presented mRNA PIEZO2 expression significantly lower than patients with spontaneous voiding. mRNA PIEZO2 expression was alike in men with and without detrusor overactivity. A positive correlation between mRNA PIEZO2 expression levels and bladder compliance was observed.
Conclusions: Our findings of PIEZO2 downregulation in the detrusor of men with benign prostatic hyperplasia, especially in those with urinary retention and those with reduced bladder compliance, suggest PIEZO2’s potential role in bladder outlet obstruction-induced bladder dysfunction. Our evaluation was restricted to the transcriptional regulation level, although translational and activity levels are critical for a comprehensive understanding. The limited size of our study population and the fact that our patients had large prostates and severe bladder outlet obstruction restricted our ability to examine any potential association between severity of obstruction and PIEZO2 expression. Further studies are necessary to elucidate the role of PIEZO mechanotransducers in the bladder and its therapeutic implications.

Palavras Chave

PIEZO 2 Channel; Bladder Outlet Obstruction; Lower Urinary Tract