Estradiol induces the rapid trafficking of membrane-associated ERá isoforms in pituitary cells

S. ZARATE; G. JAITA; J. FERRARIS; G. EIJO; M. L. MAGRI; D. PISERA; A. SEILICOVICH

Florencia

Congreso; 15º International Congress of Endocrinology; 2012

In the pituitary, estrogens regulate several cell functions via the activation of membrane-associated estrogen receptors (mERs). We have previously reported that both 17â-estradiol (E2) and membrane-impermeable E2-BSA induce rapid apoptotic actions in anterior pituitary (AP) cells, lactotropes and somatotropes through the activation of mERs. In the present study, we investigated the involvement of mERa in the apoptotic action of E2 in lactotropes. We also studied the expression of mERa variants in AP cells during the estrous cycle and the regulation of this receptor expression by E2. Cultured anterior pituitary cells from ovariectomized (OVX) Wistar rats were incubated with E2-BSA (10-9M) in the presence of an ERa selective antagonist, MPP (10-7 M), for 120 min. Apoptotic lactotropes were identified by TUNEL and immunocytochemistry for prolactin. The expression of mERa isoforms was studied in AP cells from rats at proestrus (P) or diestrus I (D) by surface biotinylation and Western Blot. The expression of mERa was also studied in AP cells from OVX rats incubated with E2 (10-9M) for 0-120 min. E2-BSA increased the percentage of TUNEL-positive lactotropes (p