17beta-estradiol stimulates the translocation of endogenous estrogen receptor á at the plasma membrane of normal pituitary cells

GUTIERREZ, S.; SOSA, L.V.; PETITI, J.P.; MUKDSI, J.H.; MASCANFRONI, I.D.; PELLIZAS, C.G.; DE PAUL, A.L.; CAMBIASSO, M.J.; TORRES, A.

MOLECULAR AND CELLULAR ENDOCRINOLOGY.

ELSEVIER IRELAND LTD

Lugar: Amsterdam, North-Holland.; Año: 2012 vol. 355 p. 169 - 179

0303-7207

Abstract In the present work we aimed at identifying ERá in the plasma membrane ofERá in the plasma membrane of normal anterior pituitary cells and investigated if 17â-estradiol was able to induce their subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the â-estradiol was able to induce their subcellular redistribution. Our results show that about 8% of anterior pituitary cells expressed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the intensity being increased after steroid hormone treatment. 17â-estradiol and the ssed ERá in the plasma membrane, with the geometrical mean fluorescence intensity being increased after steroid hormone treatment. 17â-estradiol and the17â-estradiol and the selective ERá agonist PPT induced an increase of ERá expression in the plasma membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to PPT induced an increase of ERá expression in the plasma membrane and activated the PKCá/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 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to with genomic actions, thus supporting the notion of membrane-initiated effects. These findings suggest that 17â-estradiol stimulates the translocation of endogenous ERá to á/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 17â-estradiol stimulates the translocation of endogenous ERá tosuggest that 17â-estradiol stimulates the translocation of endogenous ERá to the plasma membrane, consequently modulating this ER pool and leading to cellular biological effects in normal anterior pituitary gland.