scholarly journals Neurotrophin/receptor expression in urinary bladder of mice with overexpression of NGF in urothelium

2011 ◽  
Vol 300 (2) ◽  
pp. F345-F355 ◽  
Author(s):  
Beatrice M. Girard ◽  
Susan E. Malley ◽  
Margaret A. Vizzard
Keyword(s):  
Growth Factor ◽  
Urinary Bladder ◽  
Transgenic Mice ◽  
Protein Expression ◽  
Neurotrophic Factor ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Bladder Function ◽  
Neurotrophin Receptor ◽  
Neuronal Sprouting

Urothelium-specific overexpression of nerve growth factor (NGF) in the urinary bladder of transgenic mice stimulates neuronal sprouting in the urinary bladder, produces increased voiding frequency, and results in increased referred somatic hypersensitivity. Additional NGF-mediated pleiotropic changes might contribute to the increased voiding frequency and pelvic hypersensitivity observed in these transgenic mice, such as modulation of other growth factor/receptor systems. Chronic overexpression of NGF in the urothelium was achieved through the use of a highly urothelium-specific uroplakin II promoter. In the present study, we examined NGF, brain-derived neurotrophic factor (BDNF), and associated receptor [p75NTR, tyrosine kinase (Trk)A, TrkB] transcript and protein expression in urothelium and detrusor smooth muscle of NGF-overexpressing (OE) and littermate wild-type mice, using real-time quantitative reverse transcription-polymerase chain reaction, ELISAs, and semiquantitation of immunohistochemistry. We focused on these growth factor/receptors given the established roles of NGF/TrkA, NGF/p75NTR, and BDNF/TrkB systems in bladder function. Increased voiding frequency in NGF-OE mice was confirmed by examining urination patterns. BDNF, TrkA, and TrkB protein expression was significantly ( P ≤ 0.01) reduced and p75NTR protein expression was significantly ( P ≤ 0.01) increased in urinary bladder of NGF-OE mice. The NGF-OE-induced changes in neurotrophic factor/receptor expression in urinary bladder may represent compensatory changes to reduce voiding frequency in the NGF-OE mouse.

scholarly journals Social stress induces changes in urinary bladder function, bladder NGF content, and generalized bladder inflammation in mice

2014 ◽  
Vol 307 (7) ◽  
pp. R893-R900 ◽  
Author(s):  
Gerald C. Mingin ◽  
Abbey Peterson ◽  
Cuixia Shi Erickson ◽  
Mark T. Nelson ◽  
Margaret A. Vizzard
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Urinary Bladder ◽  
Protein Expression ◽  
Social Stress ◽  
Bladder Dysfunction ◽  
Bladder Capacity ◽  
Bladder Function ◽  
Nerve Growth ◽  
Urinary Bladder Dysfunction

Social stress may play a role in urinary bladder dysfunction in humans, but the underlying mechanisms are unknown. In the present study, we explored changes in bladder function caused by social stress using mouse models of stress and increasing stress. In the stress paradigm, individual submissive FVB mice were exposed to C57BL/6 aggressor mice directly/indirectly for 1 h/day for 2 or 4 wk. Increased stress was induced by continuous, direct/indirect exposure of FVB mice to aggressor mice for 2 wk. Stressed FVB mice exhibited nonvoiding bladder contractions and a decrease in both micturition interval (increased voiding frequency) and bladder capacity compared with control animals. ELISAs demonstrated a significant increase in histamine protein expression with no change in nerve growth factor protein expression in the urinary bladder compared with controls. Unlike stressed mice, mice exposed to an increased stress paradigm exhibited increased bladder capacities and intermicturition intervals (decreased voiding frequency). Both histamine and nerve growth factor protein expression were significantly increased with increased stress compared with control bladders. The change in bladder function from increased voiding frequency to decreased voiding frequency with increased stress intensity suggests that changes in social stress-induced urinary bladder dysfunction are context and duration dependent. In addition, changes in the bladder inflammatory milieu with social stress may be important contributors to changes in urinary bladder function.

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