Ontogenetic Changes in the Expression of Estrogen Receptor α and β in Rat Pituitary Gland Detected by Immunohistochemistry

The physiological effects of estrogen on the pituitary, including cellular proliferation and regulation of hormone synthesis, are mediated by the nuclear estrogen receptor (ER). The purpose of this study was to determine ontogenetic expression of two types of ERs (ERα and ERβ) in the pituitary using...

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Veröffentlicht in:Endocrinology (Philadelphia) 2000-02, Vol.141 (2), p.615-620
Hauptverfasser: Nishihara, Eijun, Nagayama, Yuji, Inoue, Satoshi, Hiroi, Hisahiko, Muramatsu, Masami, Yamashita, Shunichi, Koji, Takehiko
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Sprache:eng
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Zusammenfassung:The physiological effects of estrogen on the pituitary, including cellular proliferation and regulation of hormone synthesis, are mediated by the nuclear estrogen receptor (ER). The purpose of this study was to determine ontogenetic expression of two types of ERs (ERα and ERβ) in the pituitary using specific antibodies, monoclonal antibody (1D5) for ERα and polyclonal antibody generated against ERβ. First, we confirmed the detection of 66- and 55-kDa bands for ERα and ERβ, respectively, in the rat pituitary extract by Western blotting. Then immunostaining with these antibodies was performed using fetal and adult Wistar rat tissues, combined with PRL or LHβ immunohistochemistry. Intense ERβ signal was detected throughout the pituitary from day 12 of gestation. However, staining for ERα only became detectable from day 17 of gestation. In contrast with the fetal period, nuclei stained for ERα were widely distributed in the anterior lobe in the adult rat, whereas ERβ-positive cells were restricted in the anterior lobe. LHβ, but not PRL, was colocalized in ERβ-positive cells. Our results indicated that the major population of ER subtypes in the rat pituitary gland has changed around the day of birth and that the expression of ERβ may be involved in the differentiation of pituitary cell function to synthesize a specific hormone.
ISSN:0013-7227
1945-7170
DOI:10.1210/endo.141.2.7330