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

被引:7
作者
Allgeier, Sarah Hicks [2 ]
Vezina, Chad M. [1 ]
Lin, Tien-Min [1 ]
Moore, Robert W. [1 ]
Silverstone, Allen E. [3 ]
Mukai, Motoko [4 ]
Gavalchin, Jerrie [5 ]
Cooke, Paul S. [4 ]
Peterson, Richard E. [1 ,2 ]
机构
[1] Univ Wisconsin, Sch Pharm, Madison, WI 53705 USA
[2] Univ Wisconsin, Mol & Environm Toxicol Ctr, Madison, WI USA
[3] SUNY Upstate Med Univ, Dept Microbiol & Immunol, Syracuse, NY USA
[4] Univ Illinois, Dept Vet Biosci, Urbana, IL 61801 USA
[5] Cornell Univ, Dept Anim Sci, Ithaca, NY 14853 USA
关键词
Prostatic budding patterns; Estrogen signaling; 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); ICI 182,780; Estrogen receptor knockout mice; Prostate development; MOUSE VENTRAL PROSTATE; SEMINAL-VESICLE DEVELOPMENT; ARYL-HYDROCARBON RECEPTOR; IN-UTERO; SEXUAL DEVELOPMENT; C57BL/6; MICE; EXPERIMENTAL INTERSEXUALITY; REPRODUCTIVE PHENOTYPES; UROGENITAL SINUS; FETAL EXPOSURE;
D O I
10.1016/j.taap.2009.06.001
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
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. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:80 / 86
页数:7
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