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Developmental expression of glial cell‐line derived neurotrophic factor, neurturin, and their receptor mRNA in the rat urinary bladder
Author(s) -
Kawakami Takahiro,
Wakabayashi Yoshihiko,
Aimi Yoshinari,
Isono Takahiro,
Okada Yusaku
Publication year - 2002
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.10074
Subject(s) - glial cell line derived neurotrophic factor , neurturin , neurotrophic factors , proto oncogene proteins c ret , gdnf family of ligands , receptor , biology , medicine , endocrinology , microbiology and biotechnology
Aims: Glial cell‐line derived neurotrophic factor (GDNF) and related factors neurturin (NRTN), artemin, and persephin are members of the GDNF family of neurotrophic factors. GDNF and NRTN bind to the tyrosine kinase receptor Ret and the receptors GFRα1 and GFRα2. The objective was to examine the developmental expression of GDNF, NRTN, and their receptors within the rat urinary bladder. Methods: Rat bladders dissected from embryonic day (E) 15, postnatal day (P) 0, P14, P28, and adult rats (P60) were investigated by semiquantitative reverse transcriptase polymerase chain reaction. Embryos (E15, E16, and E17) were immunohistochemically stained for neurofilament. Results: GDNF and Ret mRNA levels at E15 were the highest of all the stages we examined and then immediately decreased. In contrast, NRTN mRNA levels did not change between E15 and postnatal day 14; thereafter, they gradually but insignificantly increased. GFRα1 and GFRα2 mRNA levels were high at E15, after which their signal intensities decreased. In whole‐mounted specimens, neurofilament‐positive axons were first detected in the bladder at E16. Conclusions: Our results suggest that GDNF and NRTN may act as trophic factors for neural in‐growth to the bladder and/or for the maintenance of mature neurons innervating the bladder. These factors might also be involved in bladder morphogenesis. Neurourol. Urodynam. 22:83–88, 2003. © 2003 Wiley‐Liss, Inc.