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and ERß Exhibit Unique Pharmacologic Properties When Coupled to Activation of the Mitogen-Activated Protein Kinase Pathway1
Departments of Pharmacology (C.B.W., D.M.D.) and Psychiatry and Behavioral Sciences (R.A.S., D.M.D.), and Graduate Program in Neurobiology and Behavior (S.R.), University of Washington, School of Medicine, Seattle, Washington 98195
Address all correspondence and requests for reprints to: Christian B. Wade, University of Washington, Department of Pharmacology, Box 357280, 1959 Northeast Pacific Street, Seattle, Washington 98195. E-mail: cwade{at}u.washington.edu
The rapid, nongenomic effects of estrogen are increasingly recognized
as playing an important role in several aspects of estrogen action.
Rapid activation of the mitogen-activated protein kinase (MAPK)
signaling pathway by estrogen is among the more recently identified of
these effects. To explore the role of estrogen receptors (ERs) in
mediating these effects, we have transfected ER-negative Rat-2
fibroblasts with complementary DNA clones encoding either human ER
or rat ERß and examined their ability to couple to activation of MAPK
in response to 17ß-estradiol (17ß-E2) and other
ligands. For both receptors, addition of E2 resulted
in a rapid phosphorylation of MAPK. Activation of MAPK in
ER-transfected cells was partially and completely blocked by the
antiestrogens tamoxifen and ICI 182,780, respectively. In
ERß-transfected cells, MAPK activation was less sensitive to
inhibition by tamoxifen and ICI 182,780. We have also observed that, in
this model system, a membrane-impermeable estrogen
(BSA-E2) and 17-E2 were both able
to activate MAPK in a manner similar to E2 alone. Here
also, ICI 182,780 blocked the ability of BSA-E2 to
activate MAPK through ER, but failed to block ERß-mediated
effects. BSA-E2 treatment, however, failed to activate
nuclear estrogen-response-element-mediated gene transcription. These
data show that these nuclear ERs are necessary for estrogen’s effects
at the membrane. This model system will be useful in identifying
molecular interactions involved in the rapid effects mediated by the
ERs.
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