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1 Urology, University of Pennsylvania, Philadelphia, PA, USA; Urology, Children's Hospital of Philadelphia, Philadelphia, PA, USA
2 Urology, Children's Hospital of Philadelphia, Philadelphia, PA, USA
3 Urology, University of Pennsylvania, Philadelphia, PA, USA
4 Urology, University of Pennsylvania, Philadelphia, PA, USA; Pathobiology, University of Pennsylvania, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: chackosk{at}mail.med.upenn.edu.
Partial urinary bladder outlet obstruction (PBOO) in men, secondary to benign prostatic hyperplasia, induces detrusor smooth muscle (DSM) hypertrophy. However, despite DSM hypertrophy, some bladders become severely dysfunctional (decompensated). Using a rabbit model of PBOO, we found that although DSM from sham-operated bladders expressed nearly 100% of both the smooth muscle myosin heavy chain isoform SM-B and essential light chain isoform LC17a, DSM from severely dysfunctional bladders expressed as much as 75% SM-A and 40% LC17b (both associated with decreased maximum velocity of shortening). DSM from dysfunctional bladder also exhibited tonic-type contractions, characterized by slow force generation and high force maintenance. Immunofluorescence microscopy showed decreased SM-B expression in dysfunctional bladders was not due to generation of a new cell population lacking SM-B. Metabolic cage monitoring revealed decreased void volume and increased voiding frequency correlated with overexpression of SM-A and LC17b. Myosin isoform expression and bladder function returned toward normal upon removal of the obstruction, indicating that the level of expression of these isoforms are markers of the PBOO-induced dysfunctional bladders.
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