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This version published online on August 12, 2004
Endocrinology, doi:10.1210/en.2004-0973
A more recent version of this article appeared on November 1, 2004
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*Compound via MeSH
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*ESTRADIOL

Submitted on July 27, 2004
Accepted on August 3, 2004

Glia mediates the neuroprotective action of estradiol on {beta}-amyloid-induced neuronal death

M. A. Sortino*, M. Chisari, S. Merlo, C. Vancheri, M. Caruso, F. Nicoletti, P. L. Canonico, and A. Copani

Department of Experimental and Clinical Pharmacology, Internal Medicine and Pharmaceutical Sciences, University of Catania; DISCAFF, University of Piemonte Orientale; Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Italy

* To whom correspondence should be addressed. E-mail: msortino{at}unict.it.

17{beta}-estradiol (17{beta}-E2) is known to exert neuroprotective activity against {beta}-amyloid, but its exact target and mechanism of action in this effect have not been elucidated. The involvement of astroglia in neuroprotection of 17{beta}-E2 against the {beta}-amyloid fragment {beta}AP (25-35) has been evaluated by using an experimental paradigm in which medium conditioned from rat astroglia pre-treated with 17{beta}-E2 was transferred to pure rat cortical neurons challenged with 25 µM {beta}AP (25-35) for 24 h. Toxicity of {beta}AP (25-35) was assessed by flow cytometry, evaluating the ability of the peptide to induce an aberrant mitotic cell cycle in neurons. The results obtained indicate that conditioned medium from astrocytes pre-exposed to 17{beta}-E2 for 4 h increased the viability of cortical neurons treated with {beta}AP (25-35). This effect was not modified by treatment with the estrogen receptor antagonist ICI 182,780, added directly to neurons, nor was it mimicked by direct addition of 17{beta}-E2 to neuronal cultures during exposure to {beta}AP (25-35). A soluble factor stimulated by 17{beta}-E2 seemed to be involved and, accordingly, the intracellular and released levels of transforming growth factor {beta}1 (TGF-{beta}1) were increased by 17{beta}-E2 treatment as established by Western blot analysis. In addition, the intracellular content of TGF-{beta}1 in immunopositive cells, as detected by flow cytometry, was reduced suggesting that 17{beta}-E2 stimulated mainly the release of the cytokine. In support of a role for TGF-{beta}1 in astrocyte-mediated 17{beta}-E2 neuroprotective activity, incubation with a neutralizing anti-TGF-{beta}1 antibody significantly modified the reduction of neuronal death induced by 17{beta}-E2 astrocyte conditioned medium.
Key words: cell cycle • apoptosis • transforming growth factor {beta} • astrocyte




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