Hormonal Regulation of Prolactin Cell Development in the Fetal Pituitary Gland of the Mouse
| Autor: | Sonoko Ogawa, Toshio Harigaya, Setsuji Hisano, Haruo Nogami, Mumeko C. Tsuda, Kiyomoto Ogasawara, Jan-Åke Gustafsson, Kenneth S. Korach |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2009 |
| Předmět: |
Male
endocrine system Pituitary gland medicine.medical_specialty endocrine system diseases medicine.drug_class Estrogen receptor Biology Prolactin cell chemistry.chemical_compound Mice Endocrinology Fetus Epidermal growth factor Pregnancy Internal medicine medicine Animals Estrogen Receptor beta Glucocorticoids Cells Cultured Embryonic Stem Cells Mice Knockout Mice Inbred ICR Forskolin Estradiol Estrogen Receptor alpha Cell Differentiation Embryo Mammalian Prolactin Hormones medicine.anatomical_structure chemistry Estrogen Pituitary Gland ComputingMethodologies_DOCUMENTANDTEXTPROCESSING Female hormones hormone substitutes and hormone antagonists Hormone |
| Zdroj: | Endocrinology. 150(2):1061-1068 |
| ISSN: | 0013-7227 |
| Popis: | application/pdf 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){alpha} and ERβ were expressed in the fetal pituitary gland, the results from ER knockout models showed that only ER{alpha} mediates E2 action on PRL cells. A few PRL cells were observed in ER{alpha}-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. |
| Databáze: | OpenAIRE |
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