Alteration in expression of myosin isoforms in detrusor smooth muscle following bladder outlet obstruction |
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Authors: | DiSanto Michael E Stein Raimund Chang Shaohua Hypolite Joseph A Zheng Yongmu Zderic Stephen Wein Alan J Chacko Samuel |
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Affiliation: | 3010 Ravdin-Courtyard, HUP, Univ. of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104, USA. |
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Abstract: | 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 that 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 levels of expression of these isoforms are markers of the PBOO-induced dysfunctional bladders. bladder remodeling; bladder dysfunction; SM-A; LC17a; benign prostatic hyperplasia |
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