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Endocrinology Vol. 141, No. 8 2982-2994
Copyright © 2000 by The Endocrine Society

ARTICLES

Induction of Mammary Gland Development in Estrogen Receptor-{alpha} Knockout Mice

Wayne P. Bocchinfuso, Jonathan K. Lindzey, Sylvia Curtis Hewitt, James A. Clark, Page H. Myers, Ralph Cooper and Kenneth S. Korach

Receptor Biology Section/Laboratory of Reproductive and Developmental Toxicology (W.P.B., S.C.H., K.S.K.) and Comparative Medicine Branch (J.A.C., P.H.M.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; Reproductive Toxicology Division (R.C.), Environmental Protection Agency, Research Triangle Park, North Carolina 27711; and the Department of Biology (J.K.L.), University of South Florida, Tampa, Florida 33620

Address all correspondence and requests for reprints to: Kenneth S. Korach, Ph.D., Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, MD B302, P.O. Box 12233, Research Triangle Park, NC 27709. E-mail: korach{at}niehs.nih.gov

Mammary glands from the estrogen receptor-{alpha} knockout ({alpha}ERKO) mouse do not undergo ductal morphogenesis or alveolar development. Disrupted ER{alpha} signaling may result in reduced estrogen-responsive gene products in the mammary gland or reduced mammotropic hormones that contribute to the {alpha}ERKO mammary phenotype. We report that circulating PRL is reduced in the female {alpha}ERKO mouse. Implantation of an age-matched, heterozygous ER{alpha} pituitary isograft under the renal capsule of 25-day-old or 12-week-old {alpha}ERKO mice increased circulating PRL and progesterone levels, and induced mammary gland development. Grafted {alpha}ERKO mice also possessed hypertrophied corpora lutea demonstrating that PRL is luteotropic in the {alpha}ERKO ovary. By contrast, ovariectomy at the time of pituitary grafting prevented mammary gland development in {alpha}ERKO mice despite elevated PRL levels. Hormone replacement using pellet implants demonstrated that pharmacological doses of estradiol induced limited mammary ductal elongation, and estradiol in combination with progesterone stimulated lobuloalveolar development. PRL alone or in combination with progesterone or estradiol did not induce {alpha}ERKO mammary growth. Estradiol and progesterone are required for the structural development of the {alpha}ERKO mammary gland, and PRL contributes to this development by inducing ovarian progesterone levels. Therefore, the manifestation of the {alpha}ERKO mammary phenotype appears due to the lack of direct estrogen action at the mammary gland and an indirect contributory role of estrogen signaling at the hypothalamic/pituitary axis.




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