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ORIGINAL RESEARCH ARTICLE

Downregulation of Estrogen Receptor Gene Expression by Exogenous 17ß-Estradiol in the Mammary Glands of Lactating Mice

Department of Animal Science, College of Bioresource Sciences, Nihon University, Fujisawa, Kanagawa 252-8510 Japan

To whom requests for reprints should be addressed at ¹ Department of Animal Science, College of Bioresource Sciences, Nihon University, 1866 Kameino, Fujisawa, Kanagawa 252-8510, Japan. E-mail: yamamuro{at}brs.nihon-u.ac.jp

The biological actions of estrogen are mostly conveyed through interaction with the nuclear estrogen receptor (ER). Previous evidence indicated that estrogen participates in self-regulation through the modulation of the expression of its own receptors. However, the self-regulation of estrogen against ER in the mammary gland during established lactation has not yet been investigated. The present study evaluated ER gene expression in the lactating gland activated by large doses of 17ß-estradiol (E₂). Repeated E₂ treatments dose-dependently decreased the gene expression of ER, especially its subtype ER- mRNA, which was decreased to 10% of the vehicle-injected control by 1 µg E₂ injection, whereas it was decreased by 73% for another subtype, ER-ß. A single injection of 5 µg of E₂ drastically downregulated both ER genes within 12 hrs of injection, and they did not recover to pretreatment level within 48 hrs. Western blot analysis verified that E₂ treatment inhibited the phosphorylation of Stat5, which is a potent transcriptional regulator for ER mRNA. The present findings demonstrate that E₂ treatment decreases the gene expression of its own receptor in the mammary gland during galactopoesis and induces an apparent transition of the ER profile in the mammary gland during lactation into postlactation.

Key Words: ER- • ER-ß • 17ß-estradiol • Stat5 • mammary gland • lactation

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