Dual inhibition of protein phosphatase-1/2A and calpain rescues nerve growth factor-differentiated PC12 cells from oxygen-glucose deprivation-induced cell death

2006 ◽  
Vol 83 (3) ◽  
pp. 459-468 ◽  
Author(s):  
Takayuki Nakajima ◽  
Takashi Wakasa ◽  
Yasunobu Okuma ◽  
Osamu Inanami ◽  
Yasuyuki Nomura ◽  
...  
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Protein Phosphatase ◽  
Glucose Deprivation ◽  
Protein Phosphatase 1 ◽  
Oxygen Glucose Deprivation ◽  
Differentiated Pc12 Cells ◽  
Dual Inhibition

Protective effect of L-trans-pyrrolidine-2,4-dicarboxilic acid preload against cell death induced by oxygen/glucose deprivation in differentiated PC12 cells

2005 ◽  
Vol 82 (1) ◽  
pp. 93-102 ◽  
Author(s):  
M. Elena Martín ◽  
Francisco M. Muñoz ◽  
Dale A. Dickinson ◽  
Henry Jay Forman ◽  
Rafael Martín del Río ◽  
...  
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Differentiated Pc12 Cells

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
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