NDLI: G protein-coupled estrogen receptor 1-mediated effects in the rat myometrium

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G protein-coupled estrogen receptor 1-mediated effects in the rat myometrium

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G protein-coupled estrogen receptor 1-mediated effects in the rat myometrium

Content Provider	PubMed Central
Author	Tica, Andrei A. Dun, Erica C. Tica, Oana S. Gao, Xin Arterburn, Jeffrey B. Brailoiu, G. Cristina Oprea, Tudor I. Brailoiu, Eugen
Copyright Year	2011
Abstract	G protein-coupled estrogen receptor 1 (GPER), also named GPR30, has been previously identified in the female reproductive system. In this study, GPER expression was found in the female rat myometrium by reverse transcriptase-polymerase chain reaction and immunocytochemistry. Using GPER-selective ligands, we assessed the effects of the GPER activation on resting membrane potential and cytosolic Ca2+ concentration ([Ca2+]i) in rat myometrial cells, as well as on contractility of rat uterine strips. G-1, a specific GPER agonist, induced a concentration-dependent depolarization and increase in [Ca2+]i in myometrial cells. The depolarization was abolished in Na+-free saline. G-1-induced [Ca2+]i increase was markedly decreased by nifedipine, a L-type Ca2+ channel blocker, by Ca2+-free or Na+-free saline. Intracellular administration of G-1 produced a faster and transitory increase in [Ca2+]i, with a higher amplitude than that induced by extracellular application, supporting an intracellular localization of the functional GPER in myometrial cells. Depletion of internal Ca2+ stores with thapsigargin produced a robust store-activated Ca2+ entry; the Ca2+ response to G-1 was similar to the constitutive Ca2+ entry and did not seem to involve store-operated Ca2+ entry. In rat uterine strips, administration of G-1 increased the frequency and amplitude of contractions and the area under the contractility curve. The effects of G-1 on membrane potential, [Ca2+]i, and uterine contractility were prevented by pretreatment with G-15, a GPER antagonist, further supporting the involvement of GPER in these responses. Taken together, our results indicate that GPER is expressed and functional in rat myometrium. GPER activation produces depolarization, elevates [Ca2+]i and increases contractility in myometrial cells.
Related Links	http://dx.doi.org/10.1152/ajpcell.00501.2010
Starting Page	1262
File Format	PDF
ISSN	03636143
e-ISSN	15221563
Journal	American Journal of Physiology - Cell Physiology
Issue Number	5
Volume Number	301
Language	English
Publisher	American Physiological Society
Publisher Date	2011-11-01
Access Restriction	Open
Rights Holder	American Physiological Society
Subject Keyword	Cell Biology Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

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