This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ogasawara, K. Articles by Hisano, S. Search for Related Content PubMed PubMed Citation Articles by Ogasawara, K. Articles by Hisano, S.

Hormonal Regulation of Prolactin Cell Development in the Fetal Pituitary Gland of the Mouse

Laboratory of Neuroendocrinology (K.O., H.N., S.H.), Institute of Basic Medical Sciences, and Laboratory of Behavioral Neuroendocrinology (M.C.T., S.O.), Graduate School of Comprehensive Human Sciences, University of Tsukuba, Ibaraki 305-8575, Japan; Department of Biosciences and Nutrition (J.-Å.G.), Karolinska Institute, S-14186 Huddinge, Sweden; Laboratory of Reproductive and Developmental Toxicology (K.S.K.), National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709; and Laboratory of Functional Anatomy (T.H), Faculty of Agriculture, Meiji University, Kanagawa 214-71, Japan

Address all correspondence and requests for reprints to: Haruo Nogami, Ph.D., Laboratory of Neuroendocrinology, Institute of Basic Medical Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba, Ibaraki 305-8575, Japan. E-mail: hnogami{at}md.tsukuba.ac.jp.

The developmental process of prolactin (PRL) cells in the fetal pituitary gland was studied in mice. Although PRL cells were hardly detectable in the pituitary gland of intact fetuses, a treatment with 17β-estradiol (E₂) in vitro induced a number of PRL cells that varied drastically in number depending on the stage of gestation with a peak at embryonic d 15. This effect was specific to E₂, with epidermal growth factor, insulin, and forskolin failing to induce PRL cells. Although both estrogen receptor (ER) and ERβ were expressed in the fetal pituitary gland, the results from ER knockout models showed that only ER mediates E₂ action on PRL cells. A few PRL cells were observed in ER-deficient mice as well as in their control littermates, suggesting that estrogen is not required for the phenotype determination of PRL cells. Unexpectedly, the effect of E₂ on the induction of PRL cells in vitro was diminished after embryonic d 15. Present results suggest that the exposure of fetal PRL cells to glucocorticoids (GCs) results in a reduction of sensitivity to E₂. The mechanism underlying the down-regulation of estrogen sensitivity by GCs was found not to be down-regulation of ER levels, induction of annexin 1, a GC-inducible inhibitor of PRL secretion, or a decrease in the number of PRL precursors by apoptosis. The effect of GCs appeared within 2 h and did not require a de novo protein synthesis. GCs are considered to be involved in the mechanisms of silencing pituitary PRL in gestation possibly through a novel mechanism.

This article has been cited by other articles:

				T. Hikake, S. Hayashi, T. Iguchi, and T. Sato The role of IGF1 on the differentiation of prolactin secreting cells in the mouse anterior pituitary J. Endocrinol., November 1, 2009; 203(2): 231 - 240. [Abstract] [Full Text] [PDF]