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 | |
dc.contributor.author | Radovick, Sally | |
dc.contributor.author | Huang, KuoHsiang | |
dc.contributor.author | Yu, Shengqiang | |
dc.contributor.author | Chang, Chawnshang | |
dc.contributor.author | Messing, Edward M | |
dc.contributor.author | 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 | |
dc.identifier.issn | 0013-7227 | |
dc.identifier.issn | 1945-7170 | |
dc.identifier.uri | ||
dc.language | eng | |
dc.publisher | The Endocrine Society | |
dc.relation.ispartof | Endocrinology | |
dc.relation.isversionof | 10.1210/en.2008-0044 | |
dc.subject | Prostate | |
dc.subject | Testis | |
dc.subject | Seminiferous Tubules | |
dc.subject | Animals | |
dc.subject | Mice, Knockout | |
dc.subject | Humans | |
dc.subject | Mice | |
dc.subject | Infertility, Male | |
dc.subject | Atrophy | |
dc.subject | Testosterone | |
dc.subject | Desmin | |
dc.subject | Vimentin | |
dc.subject | Fibroblast Growth Factor 2 | |
dc.subject | Estrogen Receptor alpha | |
dc.subject | Sperm Count | |
dc.subject | Reverse Transcriptase Polymerase Chain Reaction | |
dc.subject | Morphogenesis | |
dc.subject | 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 | |
pubs.organisational-group | Duke Cancer Institute | |
pubs.organisational-group | Pathology | |
pubs.organisational-group | Duke | |
pubs.organisational-group | Institutes and Centers | |
pubs.organisational-group | Clinical Science Departments | |
pubs.publication-status | Published | |
pubs.volume | 150 |