Defects of prostate development and reproductive system in the estrogen receptor-alpha null male mice.
Journal Article (Journal Article)
The estrogen receptor-alpha knockout (ERalphaKO, ERalpha-/-) mice were generated via the Cre-loxP system by mating floxed ERalpha mice with beta-actin (ACTB)-Cre mice. The impact of ERalpha gene deletion in the male reproductive system was investigated. The ACTB-Cre/ERalpha(-/-) male mice are infertile and have lost 90% of epididymal sperm when compared with wild-type mice. Serum testosterone levels in ACTB-Cre/ERalpha(-/-) male mice are 2-fold elevated. The ACTB-Cre/ERalpha(-/-) testes consist of atrophic and degenerating seminiferous tubules with less cellularity in the disorganized seminiferous epithelia. Furthermore, the ventral and dorsal-lateral prostates of ACTB-Cre/ERalpha(-/-) mice display reduced branching morphogenesis. Loss of ERalpha could also be responsible for the decreased fibroblast proliferation and changes in the stromal content. In addition, we found bone morphogenetic protein, a mesenchymal inhibitor of prostatic branching morphogenesis, is significantly up-regulated in the ACTB-Cre/ERalpha(-/-) prostates. Collectively, these results suggest that ERalpha is required for male fertility, acts through a paracrine mechanism to regulate prostatic branching morphogenesis, and is involved in the proliferation and differentiation of prostatic stromal compartment.
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Duke Authors
Cited Authors
- Chen, M; Hsu, I; Wolfe, A; Radovick, S; Huang, K; Yu, S; Chang, C; Messing, EM; Yeh, S
Published Date
- January 2009
Published In
Volume / Issue
- 150 / 1
Start / End Page
- 251 - 259
PubMed ID
- 18755802
Pubmed Central ID
- PMC5398428
International Standard Serial Number (ISSN)
- 0013-7227
Digital Object Identifier (DOI)
- 10.1210/en.2008-0044
Language
- eng
Conference Location
- United States