Progressive prostate hyperplasia in adult prolactin transgenic mice is not dependent on elevated serum androgen levels.
BACKGROUND
Transgenic mice overexpressing the rat prolactin (PRL) gene under control of the metallothionein-1 promoter (Mt-1) develop a dramatic prostatic enlargement. These animals also display significantly elevated testosterone serum levels. In this study, we aim to clarify the role of circulating androgen levels in the promotion of abnormal prostate growth in the adult PRL transgenic mouse prostate.


METHODS
Prostate morphology and androgen-receptor distribution patterns were analyzed in castrated and testosterone substituted adult PRL transgenic and in wild-type males.


RESULTS
Progressive prostatic hyperplasia in adult PRL transgenic males was not affected by substitution to serum testosterone levels corresponding to wild-type. Furthermore, prolonged testosterone treatment in adult wild-type males did not produce any significant changes in prostate growth or morphology compared with wild-type controls. Immunohistochemical studies revealed a significantly increased proportion of androgen receptor positive epithelial cells in all lobes of the PRL transgenic prostate versus wild-type.


CONCLUSIONS
The present study demonstrates that progressive prostate hyperplasia in adult PRL transgenic mice is not dependent on elevated serum androgen levels. Furthermore, prolonged androgen treatment in adult wild-type male mice appears to have no significant effect on prostate growth. In addition, our results suggest that prolonged hyperprolactinemia results in changes in prostate epithelial and stromal cell androgen receptor distribution.
Kindblom
Jon
J
Department of Pharmacology and Physiology, Göteborg University, Sweden.
Dillner
Karin
K
Ling
Charlotte
C
Törnell
Jan
J
Wennbo
Håkan
H
D000818:Animals; D004195:Disease Models, Animal; D006966:Hyperprolactinemia / Q000150:complications* / Q000662:veterinary; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D011388:Prolactin / Q000096:biosynthesis / Q000235:genetics*; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000503:physiopathology* / Q000662:veterinary; D011944:Receptors, Androgen / Q000502:physiology*; D013739:Testosterone / Q000494:pharmacology*
D011944:Receptors, Androgen; D013739:Testosterone; D011388:Prolactin