Estrogen receptors mediate rapid activation of phospholipase C pathway in the rat endometrium
Data
2011-12-20
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Siu, Erica Rosanna 
Royer, Carine
Lucas, Thais Fabiana Gameiro
Porto, Catarina Segreti
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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.
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Steroids. New York: Elsevier B.V., v. 76, n. 14, p. 1582-1589, 2011.