Defects of prostate development and reproductive system in the estrogen receptor-α null male mice

Ming Chen, Iawen Hsu, Andrew Wolfe, Sally Radovick, Kuo Hsiang Huang, Shengqiang Yu, Chawnshang Chang, Edward M. Messing, Shuyuan Yeh

Research output: Contribution to journalArticlepeer-review

Abstract

The estrogen receptor-α knockout (ERαKO, ERα -I-) mice were generated via the Cre-loxP system by mating floxed ERα mice with β-actin (ACTB)-Cre mice. The impact of ERα gene deletion in the male reproductive system was investigated. The ACTB-Cre/ERα-I- male mice are infertile and have lost 90% of epididymal sperm when compared with wild-type mice. Serum testosterone levels in ACTB-Cre/ERα-I- male mice are 2-fold elevated. The ACTB-Cre/ERα-I- 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/ERα-I- mice display reduced branching morphogenesis. Loss of ERα could also be responsible for the decreased fibroblast proliferation and changes in the stromal content. In addition, we found bonemorphogenetic protein, a mesenchymal inhibitor of prostatic branching morphogenesis, is significantly up-regulated in the ACTB-Cre/ERα -I- prostates. Collectively, these results suggest that ERα 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.

Original languageEnglish (US)
Pages (from-to)251-259
Number of pages9
JournalEndocrinology
Volume150
Issue number1
DOIs
StatePublished - Jan 2009

ASJC Scopus subject areas

  • Endocrinology

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