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. 2020 Mar 16;21(6):2024. doi: 10.3390/ijms21062024

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Physiological and pathophysiological mechanisms of estrogen (E) action on proliferation, growth and secretion of lactotropic (PRL) cells are probably largely mediated by nuclear estrogen receptor (ER) α. Membrane G-protein-coupled estrogen receptor 1 (GPER)-mediated estrogen signaling seems to be more involved in antiproliferative and apoptotic actions in the pituitary and may contribute to rapid secretion of PRL under physiological conditions. Its expression is under ERα-mediated nuclear signaling [15,59,68,69,70].