Abstract
Programmed cell death plays an integral role in neurodegenerative diseases such as Alzheimer's disease (AD). Acetylcholinesterase (AChE) was suggested to be neurotoxic in vivo and in vitro and accelerate assembly of amyloid peptide into Alzheimer's fibrils. In our experiments, we found increased AChE expression in apoptotic neuroblastoma SK-N-SH cells after long-term culture. Our results first showed that in apoptotic SK-N-SH cells, AChE aggregated in the nucleus and suppression of AChE expression with antisense oligonucleotide could save the cells from apoptosis. It was also found that caspase-3 activity was parallel with AChE activation in apoptotic SK-N-SH cells. These results suggest that AChE plays an important role in the procession of neuroblastoma cell apoptosis and favor the association between AChE and neuronal apoptosis in AD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcholinesterase / genetics
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Acetylcholinesterase / metabolism*
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Alzheimer Disease / enzymology*
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Alzheimer Disease / genetics
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / metabolism
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Apoptosis / genetics*
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Brain / enzymology*
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Brain / pathology
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Brain / physiopathology
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Caspase 3
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Caspases / metabolism
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Cell Culture Techniques
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Cell Nucleus / enzymology*
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Cell Nucleus / genetics
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Gene Expression Regulation, Enzymologic / physiology*
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Humans
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Neuroblastoma
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Neurons / enzymology*
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Neurons / pathology
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Neurons / ultrastructure
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Oligonucleotides, Antisense / pharmacology
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RNA, Messenger / metabolism
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Tumor Cells, Cultured / metabolism
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Tumor Cells, Cultured / pathology
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Tumor Cells, Cultured / ultrastructure
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Up-Regulation / physiology
Substances
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Amyloid beta-Peptides
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Oligonucleotides, Antisense
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RNA, Messenger
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Acetylcholinesterase
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CASP3 protein, human
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Caspase 3
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Caspases