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Publication : Neurotrophin/receptor expression in urinary bladder of mice with overexpression of NGF in urothelium.

First Author  Girard BM Year  2011
Journal  Am J Physiol Renal Physiol Volume  300
Issue  2 Pages  F345-55
PubMed ID  21048026 Mgi Jnum  J:168627
Mgi Id  MGI:4889143 Doi  10.1152/ajprenal.00515.2010
Citation  Girard BM, et al. (2011) Neurotrophin/receptor expression in urinary bladder of mice with overexpression of NGF in urothelium. Am J Physiol Renal Physiol 300(2):F345-55
abstractText  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 [p75(NTR), 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/p75(NTR), 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 p75(NTR) 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.
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