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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Progesterone and EGF inhibit mouse mammary gland prolactin receptor and beta-casein gene expression.

Regulation of mouse mammary gland long-form prolactin receptor (PRL-RL) mRNA levels by progesterone and epidermal growth factor (EGF) and the relationship between PRL-RL and beta-casein gene expression were examined in vivo and in vitro. PRL-RL and beta-casein mRNA levels increased approximately 6- and 15-fold from the pregnant to the lactating period, respectively, when normalized to the level of beta-actin mRNA. Ovariectomy of pregnant mice rapidly reduced the serum concentration of progesterone and increased the level of PRL-RL and beta-casein mRNAs approximately three- and fourfold compared with sham-operated animals 24 h after the operation. Injection of progesterone, but not estrogen, inhibited the increase in both mRNA levels. PRL-RL and beta-casein mRNA levels in cultured mammary epithelium increased in response to insulin, hydrocortisone, and prolactin, whereas progesterone or EGF caused inhibition. The combination of EGF and progesterone produced a greater inhibition than either hormone alone. These results indicate that both progesterone and EGF serve as negative regulators of lactogenesis.[1]


  1. Progesterone and EGF inhibit mouse mammary gland prolactin receptor and beta-casein gene expression. Nishikawa, S., Moore, R.C., Nonomura, N., Oka, T. Am. J. Physiol. (1994) [Pubmed]
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