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Endocrinology Vol. 141, No. 5 1839-1845
Copyright © 2000 by The Endocrine Society

ARTICLES

Estradiol Induces Differential Neuronal Phenotypes by Activating Estrogen Receptor {alpha} or ß1

Cesare Patrone, Giuseppe Pollio, Elisabetta Vegeto, Eva Enmark, Ivan de Curtis, J.-Å. Gustafsson and Adriana Maggi

Center Milano Molecular Pharmacology Lab, Institute of Pharmacological Sciences, University of Milan (C.P., G.P., E.V., A.M.), 20133 Milan, Italy; Departments of Medical Nutrition and Biosciences, Karolinska Institute, Novum, Huddinge University Hospital (E.E., J.-A.G.), SM186 Huddinge, Sweden; and Cell Adhesion Unit, Department of Biological and Technological Research, San Raffaele Scientific Institute (I.d.C.), 20132, Milan, Italy

Address all correspondence and requests for reprints to: Dr. Adriana Maggi, Center MPL, Institute of Pharmacological Sciences, Via Balzaretti 9, I-20133 Milan, Italy. E-mail: adriana.maggi{at}unimi.it

Estrogens are female sex steroids that have a plethora of effects on a wide range of tissues. These effects are mediated through two well characterized intracellular receptors: estrogen receptor {alpha} and ß (ER{alpha} and ERß, respectively). Because of their high structural homology, it has been argued whether these two receptors may elicit differential biochemical events in estrogen target cells. Here we examine the effect of 17ß-estradiol-dependent activation of ER{alpha} and ERß on neurite sprouting, a well known consequence of this sex hormone action in neural cells. In SK-N-BE neuroblastoma cells transfected with ER{alpha} or ERß, 17ß-estradiol induces two distinct morphological phenotypes. ER{alpha} activation results in increased length and number of neurites, whereas ERß activation modulates only neurite elongation. By the use of chimeric receptors we demonstrate that the presence of both transcription activation functions located in the NH2-terminus and COOH-terminus of the two ER proteins are necessary for maintaining the differential biological activity reported. ER{alpha}-dependent, but not ERß-dependent, morphological changes are observed only in the presence of the active form of the small G protein Rac1B.

Our data provide the first clear evidence that, in a given target cell, ER{alpha} and ERß may play distinct biological roles and support the hypothesis that 17ß-estradiol activates selected intracellular signaling pathways depending on the receptor subtype bound.




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