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*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
*ESTRADIOL
Endocrinology Vol. 142, No. 4 1669-1677
Copyright © 2001 by The Endocrine Society

ARTICLES

Estradiol Signaling via Sequestrable Surface Receptors

W. Peter M. Benten, Christian Stephan, Michèle Lieberherr and Frank Wunderlich

Division of Molecular Parasitology and Centre of Biological-Medical Research, Heinrich-Heine-University, 40225 Duesseldorf, Germany, Centre National de la Recherche Scientifique, Unité Propre de Recherche 1524, Institute National de la Recherche Agronomique, 78352 Jouy-en-Josas, France

Address all correspondence and requests for reprints to: Prof. Dr. F. Wunderlich, Division of Molecular Parasitology, Heinrich-Heine-University, Universitaetsstrasse 1, 40225 Duesseldorf, Germany. E-mail: frank.wunderlich{at}uni-duesseldorf.de

Estradiol (E2)-signaling is widely considered to be exclusively mediated through the transcription-regulating intracellular estrogen receptor (ER) {alpha} and ERß. The aim of this study was to investigate transcription-independent E2-signaling in mouse IC-21 macrophages. E2 and E2-BSA induce a rapid rise in the intracellular free Ca2+ concentration ([Ca2+]i) of Fura-2 loaded IC-21 cells as examined by spectrofluorometry. These changes in [Ca2+]i can be inhibited by pertussis toxin, but not by the ER-blockers tamoxifen and raloxifene. The E2-signaling initiated at the plasma membrane is mediated through neither ER{alpha} nor ERß, but rather through a novel G protein-coupled membrane E2-receptor as revealed by RT-PCR, flow cytometry, and confocal laser scanning microscopy. A special feature of this E2-receptor is its sequestration upon agonist stimulation. Sequestration depends on energy and temperature, and it proceeds through a clathrin- and caveolin-independent pathway.




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