Normal prostate morphology in relaxin-mutant mice
Avinash Ganesan A , Thomas Klonisch B , Jonathan T. McGuane A , Shu Feng C , Alexander I. Agoulnik C and Laura J. Parry A DA Department of Zoology, University of Melbourne, Parkville, Vic. 3010, Australia.
B Department of Human Anatomy and Cell Science, Medical Faculty, University of Manitoba, Winnipeg, MB R3E0J9, Canada.
C Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, TX 77030, USA.
D Corresponding author. Email: ljparry@unimelb.edu.au
Reproduction, Fertility and Development 21(3) 440-450 https://doi.org/10.1071/RD08133
Submitted: 9 June 2008 Accepted: 20 October 2008 Published: 4 March 2009
Abstract
The peptide hormone relaxin is expressed in the prostate gland and secreted into the seminal plasma; however, its function within the prostate has not been established. Relaxin-mutant mice (Rln–/–) were reported to have abnormal prostate morphology, but there was no prostate phenotype in relaxin receptor-mutant (Rxfp1–/–) mice. The present study aimed to verify the phenotypes in the anterior, dorsal and lateral lobes of the prostate gland of Rln–/– and Rxfp1–/– mice at different adult ages. Rln–/– mice were also treated with relaxin to evaluate the effects of exogenously administered hormone on prostate morphology. Comparisons between these three lobes of the prostate demonstrated no obvious differences in duct morphology, epithelial height or collagen density between Rln+/+ and Rln–/– mice at 2, 4, 6, 8 and 12 months of age. This was similar in Rxfp1–/– mice. Relaxin treatment did not affect morphology or epithelial cell height in the different lobes. Furthermore, prostate lobe morphology in transgenic mice overexpressing relaxin Tg(Rln) was not different from the wild-type controls. Rxfp1 was detected in the prostate throughout adult life, but there was no consistent expression of relaxin. In summary, the present study found no evidence to support a prostate phenotype in adult Rln- or Rxfp1-mutant mice.
Additional keywords: Rxfp1, transgenic.
Acknowledgements
We thank Tania Long (Department of Zoology) and Anne Truong (Baylor College of Medicine) for assistance with breeding and genotyping the mice, and Bruce Abaloz for the histology. We are grateful to Elaine Unemori and colleagues at Corthera Inc (formally BAS Medical, San Mateo, CA, USA) for the kind gift of human recombinant relaxin. We thank Dr Michael Ittmann (Baylor College of Medicine) for his advice in the prostate lobe analysis. The work was funded by an ARC Linkage Grant to L.J.P. (LP#0211545). J.T.M. was funded by the Jenny Ryan Foundation (Australia), A.I.A. by NCI (R21CA118362) and T.K. by the University of Manitoba Research Grant Program (URGP) and Manitoba Health Research Council (MHRC).
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