scholarly journals eIF4F complex disruption causes protein synthesis inhibition during hypoxia in nerve growth factor (NGF)-differentiated PC12 cells

2012 ◽  
Vol 1823 (2) ◽  
pp. 430-438 ◽  
Author(s):  
Macarena Hernández-Jiménez ◽  
M. Irene Ayuso ◽  
M. Isabel Pérez-Morgado ◽  
Eva M. García-Recio ◽  
Alberto Alcázar ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Protein Synthesis Inhibition ◽  
Nerve Growth ◽  
Synthesis Inhibition ◽  
Differentiated Pc12 Cells ◽  
Eif4f Complex

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

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Nerve Growth ◽  
Neuronal Pc12 Cells ◽  
New Protein

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.

s-Ethyl Cysteine ands-Propyl Cysteine Alleviate β-Amyloid Induced Cytotoxicity in Nerve Growth Factor Differentiated PC12 Cells

2010 ◽  
Vol 58 (11) ◽  
pp. 7104-7108 ◽  
Author(s):  
Shih-Jei Tsai ◽  
Chia-Yu Lin ◽  
Mei-Chin Mong ◽  
Mao-Wang Ho ◽  
Mei-Chin Yin
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Differentiated Pc12 Cells ◽  
Β Amyloid

Endocytosis of nerve growth factor by ‘differentiated’ PC12 cells studied by quantitative ultrastructural autoradiography

1984 ◽  
Vol 310 (2) ◽  
pp. 223-234 ◽  
Author(s):  
Anna Stieber ◽  
William F. Hickey ◽  
Ruth Hogue-Angeletti ◽  
Nicholas K. Gonatas
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Nerve Growth ◽  
Differentiated Pc12 Cells

Lysophosphatidic acid and apoptosis of nerve growth factor-differentiated PC12 cells

1998 ◽  
Vol 53 (6) ◽  
pp. 685-696 ◽  
Author(s):  
Frederick W. Holtsberg ◽  
Marion R. Steiner ◽  
Annadora J. Bruce-Keller ◽  
Jeffrey N. Keller ◽  
Mark P. Mattson ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Lysophosphatidic Acid ◽  
Nerve Growth ◽  
Differentiated Pc12 Cells
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