Abstract
In this study, we show that pretreatment with physiological concentrations (1-100 nM) of 17β-estradiol decreased apoptosis induced by ethylcholine aziridinium (AF64A), a choline toxin, in the cholinergic neuronal cell line NG108-15. These protective effects were observed after short-term (30 min) pretreatment, and were blocked by treatment with an estrogen receptor antagonist and inhibitors of phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase kinase (MEK). The protective effects were, however, not reversed by a protein synthesis inhibitor. Furthermore, we examined the effects of 17β-estradiol on choline uptake in NG108-15 cells. Although choline uptake was inhibited by a selective inhibitor of choline uptake, hemicholinium-3, it was not altered by treatment with 17β-estradiol. These results indicated that the protective effect of 17β-estradiol on AF64A-induced apoptosis could be nongenomic, and that this effect may be due to the activation of PI3K/Akt and/or MEK/extracellular signal-regulated kinase (ERK) pathways.
| Original language | English |
|---|---|
| Pages (from-to) | 9-16 |
| Number of pages | 8 |
| Journal | Brain Research |
| Volume | 1297 |
| DOIs | |
| Publication status | Published - 2009 Oct 22 |
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Keywords
- 17β-Estradiol
- AF64A
- Apoptosis
- Caspase-3
- Protection
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
- Developmental Biology
- Molecular Biology
Cite this
Effects of estrogen on AF64A-induced apoptosis in NG108-15 cells. / Kuwagata, Yusuke; Inoue, Hiroko.
In: Brain Research, Vol. 1297, 22.10.2009, p. 9-16.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effects of estrogen on AF64A-induced apoptosis in NG108-15 cells
AU - Kuwagata, Yusuke
AU - Inoue, Hiroko
PY - 2009/10/22
Y1 - 2009/10/22
N2 - In this study, we show that pretreatment with physiological concentrations (1-100 nM) of 17β-estradiol decreased apoptosis induced by ethylcholine aziridinium (AF64A), a choline toxin, in the cholinergic neuronal cell line NG108-15. These protective effects were observed after short-term (30 min) pretreatment, and were blocked by treatment with an estrogen receptor antagonist and inhibitors of phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase kinase (MEK). The protective effects were, however, not reversed by a protein synthesis inhibitor. Furthermore, we examined the effects of 17β-estradiol on choline uptake in NG108-15 cells. Although choline uptake was inhibited by a selective inhibitor of choline uptake, hemicholinium-3, it was not altered by treatment with 17β-estradiol. These results indicated that the protective effect of 17β-estradiol on AF64A-induced apoptosis could be nongenomic, and that this effect may be due to the activation of PI3K/Akt and/or MEK/extracellular signal-regulated kinase (ERK) pathways.
AB - In this study, we show that pretreatment with physiological concentrations (1-100 nM) of 17β-estradiol decreased apoptosis induced by ethylcholine aziridinium (AF64A), a choline toxin, in the cholinergic neuronal cell line NG108-15. These protective effects were observed after short-term (30 min) pretreatment, and were blocked by treatment with an estrogen receptor antagonist and inhibitors of phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase kinase (MEK). The protective effects were, however, not reversed by a protein synthesis inhibitor. Furthermore, we examined the effects of 17β-estradiol on choline uptake in NG108-15 cells. Although choline uptake was inhibited by a selective inhibitor of choline uptake, hemicholinium-3, it was not altered by treatment with 17β-estradiol. These results indicated that the protective effect of 17β-estradiol on AF64A-induced apoptosis could be nongenomic, and that this effect may be due to the activation of PI3K/Akt and/or MEK/extracellular signal-regulated kinase (ERK) pathways.
KW - 17β-Estradiol
KW - AF64A
KW - Apoptosis
KW - Caspase-3
KW - Protection
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U2 - 10.1016/j.brainres.2009.08.065
DO - 10.1016/j.brainres.2009.08.065
M3 - Article
VL - 1297
SP - 9
EP - 16
JO - Brain Research
JF - Brain Research
SN - 0006-8993
ER -