Article ID Journal Published Year Pages File Type
5858403 Reproductive Toxicology 2015 8 Pages PDF
Abstract

•Accelerated pubertal mammary gland ductal development in Bscl2−/− mice.•Delayed vaginal opening in Bscl2−/− mice.•Accelerated pubertal onset by postweaning dietary genistein exposure.•Segregated responses of mammary gland development and vaginal opening to prepubertal genistein exposure in Bscl2−/− mice.•Decreased ERβ expression in Bscl2−/− mammary gland ductal epithelium.

Berardinelli-Seip congenital lipodystrophy 2-deficient (Bscl2−/−) mice recapitulate human BSCL2 disease with lipodystrophy. Bscl2-encoded seipin is detected in adipocytes and epithelium of mammary gland. Postnatal mammary gland growth spurt and vaginal opening signify pubertal onset in female mice. Bscl2−/− females have longer and dilated mammary gland ducts at 5-week old and delayed vaginal opening. Prepubertal exposure to 500 ppm genistein diet increases mammary gland area and accelerates vaginal opening in both control and Bscl2−/− females. However, genistein treatment increases ductal length in control but not Bscl2−/− females. Neither prepubertal genistein treatment nor Bscl2-deficiency affects phospho-estrogen receptor α or progesterone receptor expression patterns in 5-week old mammary gland. Interestingly, Bscl2-deficiency specifically reduces estrogen receptor β expression in mammary gland ductal epithelium. In summary, Bscl2−/− females have accelerated postnatal mammary ductal development but delayed vaginal opening; they display segregated responses in mammary gland development and vaginal opening to prepubertal genistein treatment.

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Life Sciences Environmental Science Health, Toxicology and Mutagenesis
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