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This version published online on December 7, 2004
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2004-0066
A more recent version of this article appeared on March 1, 2005
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*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*ESTRADIOL
*TAMOXIFEN

Submitted on January 14, 2004
Accepted on November 23, 2004

ESTROGEN AND SERMs EXERT NEUROPROTECTIVE EFFECTS AND STIMULATE THE EXPRESSION OF SELADIN-1, A RECENTLY DISCOVERED ANTI-APOPTOTIC GENE, IN HUMAN NEUROBLAST LONG-TERM CELL CULTURES

Susanna Benvenuti, Paola Luciani, Gabriella Barbara Vannelli, Stefania Gelmini, Elisa Franceschi, Mario Serio, and Alessandro Peri*

Endocrine Unit (S.B., P.L., E.F., M.S., A.P.) and Clinical Biochemistry Unit (S.G.), Dept of Clinical Physiopathology, Center for Research, Transfer and High Education on Chronic, Inflammatory, Degenerative and Neoplastic Disorders, University of Florence, Florence, Italy; Dept. of Anatomy, Histology, and Forensic Medicine (G.B.V.), University of Florence, Florence, Italy

* To whom correspondence should be addressed. E-mail: a.peri{at}dfc.unifi.it.

According to the fact that Alzheimer's disease (AD) is more common in post-menopausal women, estrogen treatment has been proposed. Experimental studies, yet mostly performed using animal models, demonstrated that estrogen exerts neuroprotective effects. We previously established neuroblast long-term cell cultures from human fetal olfactory epithelium (FNC). In the present study we addressed the role of estrogen in these unique human cells, which express both the estrogen receptor (ER) {alpha} and {beta}. We found that 17{beta}-estradiol (17{beta}E2) and the SERMs raloxifene and tamoxifen exerted neuroprotective effects, which were independent on cell proliferation, by increasing resistance against {beta}-amyloid-induced toxicity, with the exception of the highest concentrations of raloxifene (10 and 100 nM). In addition, 17{beta}E2 exposure protected from oxidative-stress, reduced apoptosis, and increased the expression of the catalytic subunit of telomerase. Furthermore, we evaluated by quantitative real-time RT-PCR whether estrogen/SERMs modulate the expression of the recently discovered seladin-1 (selective Alzheimer's disease indicator) gene, which exerts neuroprotective effects and is down regulated in AD vulnerable brain regions. 17{beta}E2 (100 pM-100 nM) and SERMs (1 nM), significantly increased the amount of seladin-1 mRNA. Conversely, 10 and 100 nM raloxifene reduced the expression of seladin-1. The effect of estrogen appears mainly mediated by ER{alpha}, because the selective ER{alpha} agonist propylpyrazole-triol determined a much greater increase of seladin-1 expression than the ER{beta} agonist diarylpropionitrile. Our results add new evidence, using human neuronal cells, for a beneficial effect of estrogen in preventing neurodegenerative diseases and suggest for the first time that seladin-1 may mediate this effect.
Key words: seladin-1 • estrogen • neuronal degeneration • neuroblasts • apoptosis




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