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

dc.contributor.author

Chen, Ming

dc.contributor.author

Hsu, Iawen

dc.contributor.author

Wolfe, Andrew

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Radovick, Sally

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Huang, KuoHsiang

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Yu, Shengqiang

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Chang, Chawnshang

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Messing, Edward M

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Yeh, Shuyuan

dc.date.accessioned

2020-12-12T02:50:55Z

dc.date.available

2020-12-12T02:50:55Z

dc.date.issued

2009-01

dc.date.updated

2020-12-12T02:50:54Z

dc.description.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.

dc.identifier

en.2008-0044

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0013-7227

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1945-7170

dc.identifier.uri

https://hdl.handle.net/10161/21894

dc.language

eng

dc.publisher

The Endocrine Society

dc.relation.ispartof

Endocrinology

dc.relation.isversionof

10.1210/en.2008-0044

dc.subject

Prostate

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Testis

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Seminiferous Tubules

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Animals

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Mice, Knockout

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Humans

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Mice

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Infertility, Male

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Atrophy

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Testosterone

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Desmin

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Vimentin

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Fibroblast Growth Factor 2

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Estrogen Receptor alpha

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Sperm Count

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Reverse Transcriptase Polymerase Chain Reaction

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Morphogenesis

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Male

dc.title

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

dc.type

Journal article

duke.contributor.orcid

Chen, Ming|0000-0002-3470-1062

pubs.begin-page

251

pubs.end-page

259

pubs.issue

1

pubs.organisational-group

School of Medicine

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Duke Cancer Institute

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Pathology

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Duke

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Institutes and Centers

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Clinical Science Departments

pubs.publication-status

Published

pubs.volume

150

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