Modulation of estrogen receptors in four different target tissues: differential effects of estrogen vs progesterone. |
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| Authors: | E J Pavlik P B Coulson |
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| Affiliation: | 1. Department of Urology, University of California, 400 Parnassus Avenue, San Francisco, CA 94143, United States;2. Department of Cancer Biology and Genetics, College of Medicine, Comprehensive Cancer Center, Ohio State University, 812 Biomedical Research Tower, 460 W. 12th Avenue, Columbus, OH 43210, United States;3. Department of Pathology, Duke University Medical Center, DUMC 3712, Durham, NC 27710, United States;4. Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, 1333 Center Drive, Gainesville, FL 32610, United States;1. ETH Zurich, Animal Physiology, Institute of Agricultural Sciences, Zurich, Switzerland;2. Technische Universität München, Physiology Weihenstephan, Freising, Germany;3. University of Veterinary Medicine Hannover, Institute of Anatomy, Hannover, Germany;4. University of Veterinary Medicine Hannover, Unit for Reproductive Medicine, Hannover, Germany;5. Utrecht University, Dep. of Equine Sciences, Faculty of Vet. Med., Utrecht, The Netherlands;1. Department of Pathology, Rochester General Hospital, University of Rochester School of Medicine, Rochester, New York;2. Department of Human Development and Family Science, The University of Georgia, Athens, Georgia;3. Department of Pathology, Rutgers–New Jersey Medical School, Newark, New Jersey;1. Leuven Institute for Fertility and Embryology, Tiensevest 168, B-3000 Leuven, Belgium;2. Department of Gynecology and Obstetrics, Clinical Center of Vojvodina, Faculty of Medicine, University of Novi Sad, Novi Sad, Serbia;3. The Ritchie Centre, MIMR-PHI Institute of Medical Research, Clayton 3168, Australia;4. Department of Obstetrics and Gynecology, Monash University, Clayton 3168, Australia;5. The Division of Reproductive Health, Warwick Medical School, Coventry CV2 2DX, United Kingdom;6. Department of Gynecology, Obstetrics and Urology, Sapienza, University of Rome, Rome, Italy;1. Department of Neurosurgery, University of Alabama at Birmingham, Birmingham, Alabama, USA;2. Department of Endocrinology, University of Alabama at Birmingham, Birmingham, Alabama, USA;3. Department of Otolaryngology, University of Alabama at Birmingham, Birmingham, Alabama, USA;1. Department of Urology, University of California, 400 Parnassus Avenue, San Francisco, CA 94143, United States;2. Department of Cancer Biology and Genetics, College of Medicine, Comprehensive Cancer Center, 812 Biomedical Research Tower, 460 West 12th Avenue, Columbus, OH 43210, United States;3. Departments of Pathology and Obstetrics and Gynecology, Duke University Medical Center, Durham, NC 27710, United States |
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| Abstract: | The effect of pretreatment with estradiol-17β with or without progesterone on estradiol cytosolie receptors was investigated in 4 different target tissues from long term castrate Sprague-Dawley rats. Receptor assay was performed by hydroxylapatite adsorption and Scatchard analysis. Treatment with estradiol (0.1 μg/rat) for 48 h in vivo increased absolute cytosolic receptor concentrations per mg DNA 3–5-fold for uterine and vaginal tissue, but no increase was observed in pituitary or hypothalamic tissue. These increases in estradiol receptor concentration after 48 h of estrogen exposure should be distinguished from “replenishment” phenomenon after shorter time periods (15–20 h) which demonstrate recovery to baseline of “available” estrogen receptors.The increase in cytosolic estrogen receptors in uterine and vaginal tissue in response to estrogen is opposed by in vivo treatment with estrogen plus progesterone. This opposition cannot be explained by competition from progesterone or negative cooperative interaction with progesterone when analyzed by Scatchard plots and Hill coefficients. Deviations from linearity in Scatchard plots are not explainable in terms of positive or negative cooperativity between estrogen and progesterone. Neither estrogen stimulation of E2-R0 nor its opposition by P4 were observed in pituitary or hypothalamic target tissues. These results support the concept of a single, non-interacting binding site for estrogen on the estrogen receptor with similar Ka values for E2-R0 in all four target tissues studied. However. the uterine and vagina “response” to E2 stimulation, as measured by changes in E2-R0 binding sites. was statistically different from the response of pituitary or hypothalamic target tissue. |
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