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Volume 17, Number 2,
Issue of January 15, 1997
pp. 511-515
Copyright ©1997 Society for Neuroscience
17 -Estradiol Exerts Neuroprotective Effects on SK-N-SH
Cells
Received Sept. 23, 1996; accepted Oct. 23, 1996.
Pattie S. Green,
Jean Bishop, and
James W. Simpkins
Center for the Neurobiology of Aging and the Department of
Pharmacodynamics, University of Florida, Gainesville, Florida 32610
Estradiol (E2) has been shown to exert organizational,
neurotrophic, and neuroprotective effects in the CNS. The present study assessed the specificity of the neuroprotective effects of estradiol for the potent 17 -isomer. SK-N-SH cells from a human neuroblastoma cell line, which we have shown to be estrogen-responsive, were cultured
at low or high plating density. Then cells were exposed to 17-E2
(0.2 or 2 nM), 17 -E2 (0.2 or 2 nM), or
cholesterol, testosterone, dihydrotestosterone, progesterone, or
corticosterone (all at 2 nM). Cultures were insulted by
serum deprivation, which caused a profound loss of cells. At 1 or
2 d of serum deprivation and steroid hormone replacement, the
protection afforded cells by the steroid addition was assessed. Serum
deprivation killed ~90% of cells cultured at both low and high
plating density. Both 17- and 17-E2 provided protection of
SK-N-SH cells at either plating density. Further, a 10-fold molar
excess of tamoxifen antagonized only approximately one-third of the
neuroprotective effects of either isomer of estradiol, and a 100-fold
excess of tamoxifen had no additional effect on the neuroprotection by
17-E2. By contrast, none of the other steroids tested protected
cells from the insult of serum deprivation. These results indicate that the neuroprotective effects of estrogens are not attributable to the
general steroid structure, and the majority of the neuroprotection may
not be mediated via a tamoxifen-antagonized receptor mechanism.
Key words:
estrogens;
17-estradiol;
17-estradiol;
neuroprotection;
SK-N-SH neuroblastoma;
cell plating density;
serum
deprivation;
tamoxifen
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