Modulation of Bcl-2 expression: a potential component of estrogen protection in NT2 neurons.
Neuroprotective effects of estrogen have been demonstrated against a variety of cytotoxic insults. We present data here addressing a possible mechanism of estrogen neuroprotection in the human teratocarcinoma cell line NT2 terminally differentiated to a neuronal phenotype. Cell death induced by H2O2 or glutamate results in a dose-dependent cell death of NT2 neurons, while 24 h of estrogen pretreatment significantly enhances neuronal viability. Bcl-2 expression has been shown to reduce oxidative stress and prevent cell death. In NT2 neurons, Bcl-2 levels are dramatically elevated upon differentiation and are further enhanced with estrogen treatment. These results suggest that neuroprotective effects of estrogen may be related to increases in Bcl-2 expression.
Department of Pharmacology, University of Washington, Seattle 98195, USA.
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Rogers
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D015153:Blotting, Western; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D002454:Cell Differentiation / Q000502:physiology; D004967:Estrogens / Q000502:physiology*; D018846:Excitatory Amino Acids / Q000633:toxicity; D005786:Gene Expression Regulation / Q000235:genetics* / Q000502:physiology*; D019254:Genes, bcl-2 / Q000235:genetics*; D018698:Glutamic Acid / Q000633:toxicity; D006801:Humans; D006861:Hydrogen Peroxide / Q000633:toxicity; D009474:Neurons / Q000502:physiology*; D016877:Oxidants / Q000633:toxicity; D018384:Oxidative Stress; D014407:Tumor Cells, Cultured
D004967:Estrogens; D018846:Excitatory Amino Acids; D016877:Oxidants; D018698:Glutamic Acid; D006861:Hydrogen Peroxide