Morphological effects of oestradiol-17ß� and selective oestrogen receptor ? and ß agonists on luteinising hormone-secreting cells in tamoxifen-treated ovariectomised rats

• Autores: José C. Garrido-Gracia, Ana Gordon, Rafaela Aguilar Cañas, José García Monterde, Alfonso Blanco Rodríguez, Juana Martín de las Mulas González-Albo, José E. Sánchez Criado
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 23, Nº. 12, 2008, págs. 1453-1463
• Idioma: inglés
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  • To investigate the role played by the different rat gonadotroph oestrogen receptor (ER) pools in the effects of oestradiol-17ß (E2) on gonadectomy cells, two-week ovariectomised (OVX) rats were used. The basic experimental group of rats was injected with 3 mg of the selective ER modulator tamoxifen (TX) on days 15-20 after OVX. Groups of TX-treated OVX rats were additionally injected on days 18-20 after OVX with 10 µg oestradiol benzoate (EB), 1 mg of the selective ER? agonist propylpyrazole triol (PPT), or 1 mg of the selective ERß diarylpropionitrile (DPN). Negative and positive control groups were OVX rats injected over six days after OVX with 0.2 ml oil and EB, respectively. On day 21 after OVX, anterior pituitary glands were dissected out and divided into halves. One hemipituitary was processed for light microscopy and immunocytochemistry for ßLH subunit and progesterone receptor (PR), and the other hemipituitary for ultrastructural evaluation. Results showed that: gonadotrophs were the only pituitary cell type expressing PR; treatment with TX alone shrunk gonadectomy cells and induced both reorganization of membrane-enclosed intracellular organelles and PR expression, and treatment with DPN or EB, but not PPT, reduced the agonistic morphological effects of TX. Considering that TX activates nuclear ER?, the results indicate that activation of nuclear ER? is determinant for the reversal effects of E2 on gonadotrope morphology and PR expression, and the simultaneous activation of ERß modulates the action of ER? in an inhibitory fashion.