Estradiol (E2)-signaling is widely considered to be exclusively mediated through the transcription-regulating intracellular estrogen receptor (ER) α and ERβ. 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 ERα nor ERβ, 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.
No takes yet. Share an insight, caveat, or question.
W. Peter M. Benten (2001) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: