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Defects of prostate development and reproductive system in the estrogen receptor-alpha null male mice.
Abstract
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.
Type
Journal articleSubject
ProstateTestis
Seminiferous Tubules
Animals
Mice, Knockout
Humans
Mice
Infertility, Male
Atrophy
Testosterone
Desmin
Vimentin
Fibroblast Growth Factor 2
Estrogen Receptor alpha
Sperm Count
Reverse Transcriptase Polymerase Chain Reaction
Morphogenesis
Male
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https://hdl.handle.net/10161/21894Published Version (Please cite this version)
10.1210/en.2008-0044Publication Info
Chen, Ming; Hsu, Iawen; Wolfe, Andrew; Radovick, Sally; Huang, KuoHsiang; Yu, Shengqiang;
... Yeh, Shuyuan (2009). Defects of prostate development and reproductive system in the estrogen receptor-alpha
null male mice. Endocrinology, 150(1). pp. 251-259. 10.1210/en.2008-0044. Retrieved from https://hdl.handle.net/10161/21894.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Ming Chen
Associate Professor in Pathology
Our laboratory is interested in understanding the molecular and genetic events underlying
cancer progression and metastasis. The focus of our work is a series of genetically
engineered mouse models that faithfully recapitulate human disease. Using a combination
of mouse genetics, omics technologies, cross-species analyses and in vitro approaches,
we aim to identify cancer cell–intrinsic and –extrinsic mechanisms driving
metastatic cancer progression, with a long

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