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Biology of Reproduction 60, 1204-1210 (1999)
©Copyright 1999 Society for the Study of Reproduction, Inc.

Estrogen Responses in Bovine Fetal Uterine Cells Involve Pathways Directed by Both Estrogen Response Element and Activator Protein-11

J.R. Malayer2,a, J. Chenga, and V.M. Woodsa

a Department of Infectious Disease and Physiology, College of Veterinary Medicine, Oklahoma State University, Stillwater, Oklahoma 74078-2006

Objectives were to examine possible roles of estrogen receptor (ER) in development of the bovine uterine endometrium in the context of ER type, enhancer type, and ligand-independent activation. Expression vectors producing either ER{alpha} or ERß were introduced into fetal uterine cells from Day 110 to 120 of gestation (UBF120 cells) and into rat embryo fibroblasts (Rat-1 cells), neither of which express endogenous ER. Reporter constructs containing either an estrogen response element (ERE) or activator protein-1 (AP-1) response element were cotransfected. These reporters were also transfected into fetal uterine cells from Day 180 to 200 of gestation (UBF180 cells), which express ER. In UBF120 and Rat-1 cells transfected with either ER{alpha} or ERß, treatment with estradiol-17ß (E2) resulted in increased activity of an ERE reporter construct, but not an AP-1 element reporter construct. The antiestrogen ICI 182,780 (ICI) exhibited E2 antagonist activity with both ER{alpha} and ERß. Thus, all components were present for E2-dependent transcription from an ERE except ER; however, cells were not competent for E2-dependent transcription mediated through AP-1. In UBF180 cells, E2 treatment increased both ERE and AP-1 reporter activity. ICI exhibited E2 antagonist activity. Treatment with epidermal growth factor resulted in increased ERE reporter activity that was inhibited by ICI, indicative of ligand-independent activation of ER. These data suggest that multiple pathways for ER-mediated gene regulation occur in the developing fetal uterus and that nuclear components necessary for action of both ER{alpha} and ERß are present prior to expression of the receptor.

1 This study was supported by NIH NICHHD 34260 and USDA NRICGP 94–37206–0937.

2 Correspondence: FAX: 405 744 7110; malayer{at}okway.okstate.edu




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Bisphenol A-Induced Increase in Uterine Weight and Alterations in Uterine Morphology in Ovariectomized B6C3F1 Mice: Role of the Estrogen Receptor
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[Abstract] [Full Text] [PDF]




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Copyright © 1999 by the Society for the Study of Reproduction.