IMBECU   20882
INSTITUTO DE MEDICINA Y BIOLOGIA EXPERIMENTAL DE CUYO
Unidad Ejecutora - UE
artículos
Título:
Estradiol interacts with insulin through membrana receptors to induce an antimitogenic effect on lactotroph cells.
Autor/es:
9. GUTIÉRREZ S, DE PAUL AL, PETITO JP, SOSA L, PALMIERI C, SOAJE M, ORGNERO EM, TORRES A.
Revista:
STEROIDS
Editorial:
Elsevier
Referencias:
Lugar: Amsterdan; Año: 2008 vol. 73 p. 515 - 527
ISSN:
0039-128X
Resumen:
The signaling mechanisms of estrogens interact with those of growth factors to control the
pituitary gland functions. The contribution of the membrane bound estrogen receptor in
these actions is not fully understood. In this study, we focused on the regulatory action of
estradiol in interaction with insulin on the secretory and proliferative lactotroph cell activities
fromprimary pituitary cell cultures. Furthermore,we studied the involvement of ERK1/2,
PKC epsilon and Pit-1 in these actions. In serum free conditions, estradiol and estradiol-BSA
promoted a differential secretory activity on PRL cells but were unable to induce lactotroph
cell proliferation. However, both free and conjugated estradiol were competent arresting
the mitogenic activity promoted by insulin. Estradiol, estradiol-BSA and insulin stimuli
increased the PKC epsilon, phosphorylated ERK 1/2 and Pit-1 expression, although combined
treatments with estradiol/insulin or estradiol-BSA/insulin induced a significant reduction
in these levels, in close correlation with the decrease of lactotroph cell proliferation. The
pre-treatment with PKC inhibitor BIM significantly inhibited the ERK activation promoted by
insulin without modifying the ERK expression levels induced by estradiol or estradiol-BSA.
By immuno-electron-microscopy the alpha nuclear estrogen receptor was localized in the
plasma membrane of lactotroph cells. These findings suggest that the membrane bound ER
participates modulating lactotroph cells proliferation via PKC epsilon, ERK1/2 and Pit-1. The
interactions between estradiol and growth factors, inducing both mitogenic and antimitogenic
effects, could provide glandular plasticity preventing an over-proliferation induced by
growth factors.