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Defects of Prostate Development and Reproductive System in the Estrogen Receptor- Null Male Mice

Departments of Urology and Pathology, University of Rochester Medical Center (M.C., I.H., K.H., S.Y., C.C., E.M.M., S.Y.), Rochester, New York 14642; and Department of Pediatrics, Johns Hopkins University College of Medicine (A.W., S.R.), Baltimore, Maryland 21287

Address all correspondence and requests for reprints to: Dr. Shuyuan Yeh, Department of Urology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 656, Rochester, New York 14642. E-mail: shuyuan_yeh{at}urmc.rochester.edu.

The estrogen receptor- knockout (ERKO, ER^–/–) mice were generated via the Cre-loxP system by mating floxed ER mice with β-actin (ACTB)-Cre mice. The impact of ER gene deletion in the male reproductive system was investigated. The ACTB-Cre/ER^–/– male mice are infertile and have lost 90% of epididymal sperm when compared with wild-type mice. Serum testosterone levels in ACTB-Cre/ER^–/– male mice are 2-fold elevated. The ACTB-Cre/ER^–/– 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/ER^–/– mice display reduced branching morphogenesis. Loss of ER 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/ER^–/– prostates. Collectively, these results suggest that ER 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.