Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5858403 | Reproductive Toxicology | 2015 | 8 Pages |
â¢Accelerated pubertal mammary gland ductal development in Bscl2â/â mice.â¢Delayed vaginal opening in Bscl2â/â mice.â¢Accelerated pubertal onset by postweaning dietary genistein exposure.â¢Segregated responses of mammary gland development and vaginal opening to prepubertal genistein exposure in Bscl2â/â mice.â¢Decreased ERβ expression in Bscl2â/â mammary gland ductal epithelium.
Berardinelli-Seip congenital lipodystrophy 2-deficient (Bscl2â/â) 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. Bscl2â/â 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 Bscl2â/â females. However, genistein treatment increases ductal length in control but not Bscl2â/â 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, Bscl2â/â 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.