INICSA   23916
INSTITUTO DE INVESTIGACIONES EN CIENCIAS DE LA SALUD
Unidad Ejecutora - UE
artículos
Título:
17beta-estradiol stimulates the translocation of endogenous estrogen receptor á at the plasma membrane of normal anterior pituitary cells
Autor/es:
GUTIERREZ SILVINA; SOSA LILIANA; PETITI JUAN PABLO; MUKDSI JORGE; MASCANFRONI IVáN; PELLIZAS CLAUDIA; DE PAUL ANA LUCIA; CAMBIASSO MARIA JULIA; TORRES ALICIA
Revista:
MOLECULAR AND CELLULAR ENDOCRINOLOGY.
Editorial:
ELSEVIER IRELAND LTD
Referencias:
Lugar: Amsterdam; Año: 2012 vol. 355 p. 169 - 169
ISSN:
0303-7207
Resumen:
In the present work we aimed at identifying ERa in the plasma membrane of normal anterior pituitary cells and investigated if 17b-estradiol was able to induce their subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERa in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17b-Estradiol and the selective ERa agonist PPT induced an increase of ERa expression in the plasma membrane and activated the PKCa/ERK 1/2 pathway in a time-course not compatible with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17b-estradiol stimulates the translocation of endogenous ERa to the plasma membrane, consequently modulating this ER pool and leading to cellular biological effects in normal anterior pituitary gland.a in the plasma membrane of normal anterior pituitary cells and investigated if 17b-estradiol was able to induce their subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERa in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17b-Estradiol and the selective ERa agonist PPT induced an increase of ERa expression in the plasma membrane and activated the PKCa/ERK 1/2 pathway in a time-course not compatible with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17b-estradiol stimulates the translocation of endogenous ERa to the plasma membrane, consequently modulating this ER pool and leading to cellular biological effects in normal anterior pituitary gland.
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