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Estrogen attenuates cell death induced by carboxy‐terminal fragment of amyloid precursor protein in PC12 through a receptor‐dependent pathway
Author(s) -
Chae HeeSun,
Bach JaeHyung,
Lee MyoungWoo,
Kim HyeSun,
Kim YongSik,
Kim Kyung Yong,
Choo Kwan Young,
Choi Se Hoon,
Park CheolHyoung,
Lee Sang Hyung,
Suh YooHun,
Kim Sung Su,
Lee Won Bok
Publication year - 2001
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.1167
Subject(s) - estrogen , estrogen receptor , tamoxifen , programmed cell death , receptor , chemistry , estrogen receptor beta , antagonist , selective estrogen receptor modulator , estrogen receptor alpha , medicine , endocrinology , pharmacology , apoptosis , biology , biochemistry , cancer , breast cancer
Abstract In the present study, we investigated effects of estrogen on cell death induced by carboxy‐terminal fragment of amyloid precursor protein (CT), a candidate causative substance in the pathogenesis of Alzheimer's disease. 17β‐Estradiol attenuated CT‐induced cell death in PC12 cells, whereas 17α‐estradiol, nonestrogenic stereoisomer, did not exert any significant protective effect on CT‐induced cell death. These results suggest that protective effects of estrogen may be mediated by estrogen receptor (ER) in PC12 cells. To confirm the results, we determined the effects of tamoxifen, an estrogen receptor antagonist. Tamoxifen blocked the protective effects of 17β‐estradiol, although it did not affect those of 17α‐estradiol. Overall, it might be thought that the protective effect of estradiol on CT‐induced cell death is achieved by hormonal properties mediated through the estrogen receptor rather than the structural properties as a reducing agent. J. Neurosci. Res. 65:403–407, 2001. © 2001 Wiley‐Liss, Inc.