Artigo
Estrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometrium
Fecha
2011-12-20Registro en:
Steroids. New York: Elsevier B.V., v. 76, n. 14, p. 1582-1589, 2011.
0039-128X
10.1016/j.steroids.2011.09.013
WOS:000298273300010
Autor
Konigame, Vivian Cristina
Siu, Erica Rosanna [UNIFESP]
Royer, Carine [UNIFESP]
Lucas, Thais Fabiana Gameiro [UNIFESP]
Porto, Catarina Segreti [UNIFESP]
Abdalla, Fernando Mauricio Francis
Institución
Resumen
The aim of the present study was to investigate the activation of rapid signaling events by 17 beta-estradiol in the rat uterus. 17 beta-Estradiol induced a rapid increase of total [(3)H]-inositol phosphate accumulation in the whole uterus and endometrium, but not in the myometrium. the effect of 17 beta-estradiol in the endometrium was blocked by phospholipase C (PLC) inhibitor (1173122), estrogen receptors antagonist (ICI 182,780), exportin CRM1 inhibitor (leptomycin B) and selective inhibitor of the SRC family of protein tyrosine kinases (PP2). Furthermore, a selective agonist of ESR1 (PPT) and a selective agonist of GPER (G-1) also induced a rapid increase of total ((3)H]-inositol phosphate accumulation in the endometrium. the G-1 effects were blocked by GPER antagonist (G-15). 17 beta-Estradiol and G-1 promoted an additive effect on total [(3)H]-inositol phosphate accumulation. in conclusion, the present results indicate that a rapid activation of the PLC-mediated phosphoinositide hydrolysis occurred in the rat endometrium after 17 beta-estradiol stimulation, and this effect was mediated by ESR1 that underwent nuclear export after hormone stimulation, and that GPER activation may play an additive role for this response. These rapid actions might be one of the key steps that mediate the estrogen-dependent activation of cellular events in the endometrium. (C) 2011 Elsevier Inc. All rights reserved.