Background: Although progress has been made in the treatment
of stress urinary incontinence (SUI), our understanding of its
etiology underlying the condition is poor.
Objective: We examined structural components and the role of
TGF-β1/Smad pathway in the urethra by parturition-induced
stress urinary incontinence. Design, setting, and participants:
Forty 8-week-old Sprague-Dawley female rats at gestational day 16 were used and immediately after delivery, the rats underwent
vaginal balloon dilation for 4 hours. One week later, the rats were
anesthetized and both ovaries were excised.
Measurements: One month later after ovariectomy, Conscious
cystometry and Leak-Point Pressure (LPP) were measured
by MP150. Multiple cystometric variables were recorded by
obtaining mean values of five voiding cycles. Histological
examination (Masson's trichrome stain, picrosirius red
stain, Hart's elastin stain, Gordon & Sweet's stain and
immunohistochemical stain) and western blot were performed
followed by urodynamic assays.
Results and Limitations: Four weeks after ovariectomy, SUI
was noted in seventeen of 20 experimental rats. The urethras of
SUI rats have more extracellular matrix (ECM) and less muscle.
Total collagen fiber and reticular fiber from SUI rats are more
than control rats. Meanwhile elastic fibers and reticular fibers
showed fragmentized and disorganized which mean the fibrousmuscular
system of SUI rats was impaired. The expression of
TGF-β1 and Smad2 protein and activity of Smad2 evaluated by
immunohistochemistry and western blot was higher in SUI rats
than in control rats.
Conclusions: The fibrous-muscular system of urethra was
impaired in SUI rats. Upregulation of TGF-β1 and Smad2 and
activation of Smad2 signaling pathway in the urethra of SUI
rats might play important role in parturition-induced structural
changes and deterioration of urethra closing pressure.