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Title: Estrogen signaling is not required for prostatic bud patterning or for its disruption by 2,3,7,8-tetrachlorodibenzo-p-dioxin

Abstract

Estrogens play an important role in prostatic development, health, and disease. While estrogen signaling is essential for normal postnatal prostate development, little is known about its prenatal role in control animals. We tested the hypothesis that estrogen signaling is needed for normal male prostatic bud patterning. Budding patterns were examined by scanning electron microscopy of urogenital sinus epithelium from wild-type mice, mice lacking estrogen receptor (ER){alpha}, ER{beta}, or both, and wild-type mice exposed to the antiestrogen ICI 182,780. Budding phenotypes did not detectably differ among any of these groups, strongly suggesting that estrogen signaling is not needed to establish the prototypical prostatic budding pattern seen in control males. This finding contributes to our understanding of the effects of low-level estrogen exposure on early prostate development. In utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can greatly alter the pattern in which prostatic buds form and reduce their number. For several reasons, including a prior observation that inhibitory effects of TCDD on prostatic budding in rats depend heavily on the sex of adjacent fetuses, we tested the hypothesis that estrogen signaling is needed for TCDD to disrupt prostatic budding. However, budding did not detectably differ among wild-type mice, or mice lacking ER{alpha}, ER{beta}, ormore » both, that were exposed prenatally to TCDD (5 {mu}g/kg on embryonic day 13.5). Nor did ICI 182,780 detectably affect the response to TCDD. These results strongly suggest that estrogen signaling is not needed for TCDD to inhibit prostatic epithelial budding.« less

Authors:
 [1]; ; ;  [2];  [3];  [4];  [5];  [4];  [1];  [6]
  1. Molecular and Environmental Toxicology Center, University of Wisconsin, Madison, WI (United States)
  2. School of Pharmacy, University of Wisconsin, Madison, WI (United States)
  3. Department of Microbiology and Immunology, SUNY Upstate Medical University, Syracuse, NY (United States)
  4. Department of Veterinary Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL (United States)
  5. Department of Animal Science, Cornell University, Ithaca, NY (United States)
  6. (United States), E-mail: repeterson@pharmacy.wisc.edu
Publication Date:
OSTI Identifier:
21272630
Resource Type:
Journal Article
Journal Name:
Toxicology and Applied Pharmacology
Additional Journal Information:
Journal Volume: 239; Journal Issue: 1; Other Information: DOI: 10.1016/j.taap.2009.06.001; PII: S0041-008X(09)00229-4; Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0041-008X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; DIOXIN; EPITHELIUM; ESTROGENS; FETUSES; HYPOTHESIS; MICE; ORGANIC CHLORINE COMPOUNDS; PROSTATE; RATS; RECEPTORS; SCANNING ELECTRON MICROSCOPY

Citation Formats

Allgeier, Sarah Hicks, Vezina, Chad M., Lin, T.-M., Moore, Robert W., Silverstone, Allen E., Mukai, Motoko, Gavalchin, Jerrie, Cooke, Paul S., Peterson, Richard E., and School of Pharmacy, University of Wisconsin, Madison, WI. Estrogen signaling is not required for prostatic bud patterning or for its disruption by 2,3,7,8-tetrachlorodibenzo-p-dioxin. United States: N. p., 2009. Web. doi:10.1016/j.taap.2009.06.001.
Allgeier, Sarah Hicks, Vezina, Chad M., Lin, T.-M., Moore, Robert W., Silverstone, Allen E., Mukai, Motoko, Gavalchin, Jerrie, Cooke, Paul S., Peterson, Richard E., & School of Pharmacy, University of Wisconsin, Madison, WI. Estrogen signaling is not required for prostatic bud patterning or for its disruption by 2,3,7,8-tetrachlorodibenzo-p-dioxin. United States. doi:10.1016/j.taap.2009.06.001.
Allgeier, Sarah Hicks, Vezina, Chad M., Lin, T.-M., Moore, Robert W., Silverstone, Allen E., Mukai, Motoko, Gavalchin, Jerrie, Cooke, Paul S., Peterson, Richard E., and School of Pharmacy, University of Wisconsin, Madison, WI. Sat . "Estrogen signaling is not required for prostatic bud patterning or for its disruption by 2,3,7,8-tetrachlorodibenzo-p-dioxin". United States. doi:10.1016/j.taap.2009.06.001.
@article{osti_21272630,
title = {Estrogen signaling is not required for prostatic bud patterning or for its disruption by 2,3,7,8-tetrachlorodibenzo-p-dioxin},
author = {Allgeier, Sarah Hicks and Vezina, Chad M. and Lin, T.-M. and Moore, Robert W. and Silverstone, Allen E. and Mukai, Motoko and Gavalchin, Jerrie and Cooke, Paul S. and Peterson, Richard E. and School of Pharmacy, University of Wisconsin, Madison, WI},
abstractNote = {Estrogens play an important role in prostatic development, health, and disease. While estrogen signaling is essential for normal postnatal prostate development, little is known about its prenatal role in control animals. We tested the hypothesis that estrogen signaling is needed for normal male prostatic bud patterning. Budding patterns were examined by scanning electron microscopy of urogenital sinus epithelium from wild-type mice, mice lacking estrogen receptor (ER){alpha}, ER{beta}, or both, and wild-type mice exposed to the antiestrogen ICI 182,780. Budding phenotypes did not detectably differ among any of these groups, strongly suggesting that estrogen signaling is not needed to establish the prototypical prostatic budding pattern seen in control males. This finding contributes to our understanding of the effects of low-level estrogen exposure on early prostate development. In utero exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can greatly alter the pattern in which prostatic buds form and reduce their number. For several reasons, including a prior observation that inhibitory effects of TCDD on prostatic budding in rats depend heavily on the sex of adjacent fetuses, we tested the hypothesis that estrogen signaling is needed for TCDD to disrupt prostatic budding. However, budding did not detectably differ among wild-type mice, or mice lacking ER{alpha}, ER{beta}, or both, that were exposed prenatally to TCDD (5 {mu}g/kg on embryonic day 13.5). Nor did ICI 182,780 detectably affect the response to TCDD. These results strongly suggest that estrogen signaling is not needed for TCDD to inhibit prostatic epithelial budding.},
doi = {10.1016/j.taap.2009.06.001},
journal = {Toxicology and Applied Pharmacology},
issn = {0041-008X},
number = 1,
volume = 239,
place = {United States},
year = {2009},
month = {8}
}