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

Journal Article · Sat Aug 15 04:00:00 EDT 2009 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/j.taap.2009.06.001· OSTI ID:21272630

Allgeier, Sarah Hicks ^[1]; Vezina, Chad M; Lin, T -M; Moore, Robert W ^[2]; Silverstone, Allen E ^[3]; Mukai, Motoko ^[4]; Gavalchin, Jerrie ^[5]; Cooke, Paul S ^[4]; Peterson, Richard E ^[1]

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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)

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.

• OSTI ID: 21272630
• Journal Information: Toxicology and Applied Pharmacology, Journal Name: Toxicology and Applied Pharmacology Journal Issue: 1 Vol. 239; ISSN TXAPA9; ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
DIOXIN
EPITHELIUM
ESTROGENS
FETUSES
HYPOTHESIS
MICE
ORGANIC CHLORINE COMPOUNDS
PROSTATE
RATS
RECEPTORS
SCANNING ELECTRON MICROSCOPY