@article{taylor_cowin_couse_korach_risbridger_2006, title={17 beta-Estradiol induces apoptosis in the developing rodent prostate independently of ER alpha or ER beta}, volume={147}, ISSN={["1945-7170"]}, DOI={10.1210/en.2005-0683}, abstractNote={Estrogens induce both proliferative and antiproliferative responses in the prostate gland. To date, antiproliferative effects of estrogens are generally considered to be due to systemic antiandrogenic actions. However, estrogen action mediated through estrogen receptor (ER) β was recently suggested as another mechanism of induction of apoptosis in the prostate. This study aimed to explore the hypothesis that the antiproliferative effects of estrogen are directly mediated through ERβ using a prostate organ culture system. We previously reported effects of 17β-estradiol (E2) using rat ventral prostate (VP) tissues, and adapted the system for culturing mouse tissues. In both rat and mouse models, estrogen-induced apoptosis was detected that was spatially and regionally localized to the epithelium of the distal tips. Using organ cultures of αER knockout (αERKO) and βERKO prostates, we failed to demonstrate that apoptosis induced by E2 was mediated through either receptor subtype. Activation of ER-selective ligands (ERα, propyl pyrazole triol, ERβ, diaryl-proprionitrile, and 5α-androstane-3β,17β-diol) in organ culture experiments failed to induce apoptosis, as did the membrane impermeable conjugate E2:BSA, discounting the possibility of nongenomic effects. Consequently, E2 regulation of androgen receptor (AR) expression was examined and, in the presence of nanomolar testosterone levels, E2 caused a specific reduction in AR protein expression in wild-type, αERKO, and βERKO mice, particularly in the distal region where apoptosis was detected. This down-regulation of AR protein provides a possible mechanism for the proapoptotic action of E2 that is independent of ERs or nongenomic effects.}, number={1}, journal={ENDOCRINOLOGY}, author={Taylor, RA and Cowin, P and Couse, JF and Korach, KS and Risbridger, GP}, year={2006}, month={Jan}, pages={191–200} }
 @article{couse_korach_2004, title={Estrogen receptor-alpha-mediates the detrimental effects of neonatal diethylstilbestrol (DES) exposure in the murine reproductive tract}, volume={205}, number={02-Jan}, journal={Toxicology (Amsterdam, Netherlands)}, author={Couse, J. F. and Korach, K. S.}, year={2004}, pages={55–63} }
 @article{couse_yates_sanford_nyska_nilson_korach_2004, title={Formation of cystic ovarian follicles associated with elevated luteinizing hormone requires estrogen receptor-beta}, volume={145}, ISSN={["1945-7170"]}, DOI={10.1210/en.2004-0548}, abstractNote={Abstract}, number={10}, journal={ENDOCRINOLOGY}, author={Couse, JF and Yates, MM and Sanford, R and Nyska, A and Nilson, JH and Korach, KS}, year={2004}, month={Oct}, pages={4693–4702} }
 @article{couse_yates_walker_korach_2003, title={Characterization of the hypothalamic-pituitary-gonadal axis in estrogen receptor (ER) null mice reveals hypergonadism and endocrine sex reversal in females lacking ER alpha but not ER beta}, volume={17}, number={6}, journal={Molecular Endocrinology (Baltimore, Md.)}, author={Couse, J. F. and Yates, M. M. and Walker, V. R. and Korach, K. S.}, year={2003}, pages={1039–1053} }
 @article{jefferson_couse_padilla-banks_korach_newbold_2002, title={Neonatal exposure to genistein induces estrogen receptor (ER)alpha expression and multioocyte follicles in the maturing mouse ovary: Evidence for ER beta-mediated and nonestrogenic actions}, volume={67}, DOI={10.1095/biolreprod.102.005371}, number={4}, journal={Biology of Reproduction}, author={Jefferson, W. N. and Couse, J. F. and Padilla-Banks, E. and Korach, K. S. and Newbold, R. R.}, year={2002}, pages={1285–1296} }
 @inbook{couse_korach_2001, title={Contrasting phenotypes in reproductive tissues of female estrogen receptor null mice}, volume={948}, number={2001}, booktitle={Environmental hormones: The scientific basis of endocrine disruption}, publisher={New York, NY: New York Academy of Sciences}, author={Couse, J. F. and Korach, K. S.}, year={2001}, pages={1–8} }
 @article{prins_birch_couse_choi_katzenellenbogen_korach_2001, title={Estrogen imprinting of the developing prostate gland is mediated through stromal estrogen receptor alpha: Studies with alpha ERKO and beta ERKO mice}, volume={61}, number={16}, journal={Cancer Research}, author={Prins, G. S. and Birch, L. and Couse, J. F. and Choi, I. and Katzenellenbogen, B. and Korach, K. S.}, year={2001}, pages={6089–6097} }
 @article{couse_dixon_yates_moore_ma_maas_korach_2001, title={Estrogen receptor-alpha knockout mice exhibit resistance to the developmental effects of neonatal diethylstilbestrol exposure on the female reproductive tract}, volume={238}, ISSN={["1095-564X"]}, DOI={10.1006/dbio.2001.0413}, abstractNote={Abstract Data indicate that estrogen-dependent and -independent pathways are involved in the teratogenic/carcinogenic syndrome that follows developmental exposure to 17β-estradiol or diethylstilbestrol (DES), a synthetic estrogen. However, the exact role and extent to which each pathway contributes to the resulting pathology remain unknown. We employed the αERKO mouse, which lacks estrogen receptor-α (ERα), to discern the role of ERα and estrogen signaling in mediating the effects of neonatal DES exposure. The αERKO provides the potential to expose DES actions mediated by the second known ER, ERβ, and those that are ER-independent. Wild-type and αERKO females were treated with vehicle or DES (2 μg/pup/day for Days 1–5) and terminated after 5 days and 2, 4, 8, 12, and 20 months for biochemical and histomorphological analyses. Assays for uterine expression of the genes Hoxa10, Hoxa11, and Wnt7a shortly after treatment indicated significant decreases in DES-treated wild-type but no effect in the αERKO. In contrast, the DES effect on uterine expression of Wnt4 and Wnt5a was preserved in both genotypes, suggesting a developmental role for ERβ. Adult αERKO mice exhibited complete resistance to the chronic effects of neonatal DES exposure exhibited in treated wild-type animals, including atrophy, decreased weight, smooth muscle disorganization, and epithelial squamous metaplasia in the uterus; proliferative lesions of the oviduct; and persistent vaginal cornification. Therefore, the lack of DES effects on gene expression and tissue differentiation in the αERKO provides unequivocal evidence of an obligatory role for ERα in mediating the detrimental actions of neonatal DES exposure in the murine reproductive tract.}, number={2}, journal={DEVELOPMENTAL BIOLOGY}, author={Couse, JF and Dixon, D and Yates, M and Moore, AB and Ma, L and Maas, R and Korach, KS}, year={2001}, month={Oct}, pages={224–238} }
 @article{couse_mahata_eddy_korach_2001, title={Molecular mechanism of estrogen action in the male: insights from the estrogen receptor null mice}, volume={13}, ISSN={["1031-3613"]}, DOI={10.1071/RD00128}, abstractNote={
Until recently, 17β-estradiol was thought to be of little importance
in male fertility. However, the descriptions of testicular dysfunction and
behavioral deficits leading to complete infertility in male mice lacking
estrogen receptor α (ERα) have indicated the importance of
estrogen action in fertility of the male rodent. In contrast, male mice
lacking the newly discovered estrogen receptor β (ERβ)
exhibit no compromised fertility. Recently, elaborate sperm transplantation
studies have shown that the altered sperm function characteristic of the
ERα knockout male are the result of the loss of ERα
actions in the supporting somatic cells of the testis and epididymis rather
than in the germ cell. This brief review will discuss the roles of estrogen
action in male reproduction as revealed by mice lacking both known forms of
the ER. A brief review of the estrogen signaling system is also included.
}, number={4}, journal={REPRODUCTION FERTILITY AND DEVELOPMENT}, author={Couse, JF and Mahata, D and Eddy, EM and Korach, KS}, year={2001}, pages={211–219} }