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Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.
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MedLine Citation:
PMID:  1469055     Owner:  NLM     Status:  MEDLINE    
Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.
P W Mesner; T R Winters; S H Green
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of cell biology     Volume:  119     ISSN:  0021-9525     ISO Abbreviation:  J. Cell Biol.     Publication Date:  1992 Dec 
Date Detail:
Created Date:  1993-01-27     Completed Date:  1993-01-27     Revised Date:  2010-09-07    
Medline Journal Info:
Nlm Unique ID:  0375356     Medline TA:  J Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1669-80     Citation Subset:  IM    
Department of Biology, University of Iowa, Iowa City 52242.
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MeSH Terms
Anisomycin / pharmacology
Apoptosis / drug effects,  physiology*
Aurintricarboxylic Acid / pharmacology
Cell Differentiation
Cell Separation
DNA Damage
Dactinomycin / pharmacology
Deoxyglucose / metabolism
Nerve Growth Factors / pharmacology*
Neurons / physiology*
PC12 Cells / drug effects,  physiology*
Protein Biosynthesis
Rats, Inbred Strains
Rats, Wistar
Sympathetic Nervous System / physiology*
Transcription, Genetic
Grant Support
Reg. No./Substance:
0/Nerve Growth Factors; 154-17-6/Deoxyglucose; 22862-76-6/Anisomycin; 4431-00-9/Aurintricarboxylic Acid; 50-76-0/Dactinomycin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): J Cell Biol
Journal ID (publisher-id): J. Cell Biol.
ISSN: 0021-9525
ISSN: 1540-8140
Publisher: The Rockefeller University Press
Article Information
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Print publication date: Day: 2 Month: 12 Year: 1992
Volume: 119 Issue: 6
First Page: 1669 Last Page: 1680
ID: 2289741
Publisher Id: 93107166
PubMed Id: 1469055

Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons

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