Induction of Bip mRNA upon Programmed Cell Death of Differentiated PC12 Cells as Well as Rat Sympathetic Neurons

1997 ◽  
Vol 121 (1) ◽  
pp. 122-127 ◽  
Author(s):  
T. Aoki ◽  
T. Koike ◽  
T. Nakano ◽  
K. Shibahara ◽  
S. Kondo ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
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.

3,4,5-Tricaffeoylquinic Acid Attenuates Proteasome Inhibition-Mediated Programmed Cell Death in Differentiated PC12 cells

2014 ◽  
Vol 39 (8) ◽  
pp. 1416-1425
Author(s):  
Yoon Jeong Nam ◽  
Da Hee Lee ◽  
Yun Jeong Kim ◽  
Yong Kyoo Shin ◽  
Dong Suep Sohn ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Proteasome Inhibition ◽  
Differentiated Pc12 Cells

Rat TAFII31Gene Is Induced upon Programmed Cell Death in Differentiated PC12 Cells Deprived of NGF

1997 ◽  
Vol 234 (1) ◽  
pp. 230-234 ◽  
Author(s):  
Tomokazu Aoki ◽  
Tatsuro Koike ◽  
Toru Nakano ◽  
Keiichi Shibahara ◽  
Hiroyuki Nishimura ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Differentiated Pc12 Cells

Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells

2001 ◽  
Vol 78 (3) ◽  
pp. 600-610 ◽  
Author(s):  
Su Ryeon Seo ◽  
Seon Ah Chong ◽  
Syng-Ill Lee ◽  
Jee Young Sung ◽  
Young Soo Ahn ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pc12 Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Erk Activation ◽  
Differentiated Pc12 Cells

scholarly journals Aurintricarboxylic acid rescues PC12 cells and sympathetic neurons from cell death caused by nerve growth factor deprivation: correlation with suppression of endonuclease activity.

1991 ◽  
Vol 115 (2) ◽  
pp. 461-471 ◽  
Author(s):  
A Batistatou ◽  
L A Greene
Keyword(s):  
Cell Death ◽  
Nerve Growth Factor ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Endonuclease Activity ◽  
Term Survival ◽  
Serum Free

Past studies have shown that serum-free cultures of PC12 cells are a useful model system for studying the neuronal cell death which occurs after neurotrophic factor deprivation. In this experimental paradigm, nerve growth factor (NGF) rescues the cells from death. It is reported here that serum-deprived PC12 cells manifest an endonuclease activity that leads to internucleosomal cleavage of their cellular DNA. This activity is detected within 3 h of serum withdrawal and several hours before any morphological sign of cell degeneration or death. NGF and serum, which promote survival of the cells, inhibit the DNA fragmentation. Aurintricarboxylic acid (ATA), a general inhibitor of nucleases in vitro, suppresses the endonuclease activity and promotes long-term survival of PC12 cells in serum-free cultures. This effect appears to be independent of macromolecular synthesis. In addition, ATA promotes long-term survival of cultured sympathetic neurons after NGF withdrawal. ATA neither promotes nor maintains neurite outgrowth. It is hypothesized that the activation of an endogenous endonuclease could be responsible for neuronal cell death after neurotrophic factor deprivation and that growth factors could promote survival by leading to inhibition of constitutively present endonucleases.

Biochemical characterization of programmed cell death in NGF-deprived sympathetic neurons

1992 ◽  
Vol 23 (9) ◽  
pp. 1205-1220 ◽  
Author(s):  
David P. Martin ◽  
Akira Ito ◽  
Kazuhiko Horigome ◽  
Patricia A. Lampe ◽  
Eugene M. Johnson
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Biochemical Characterization ◽  
Sympathetic Neurons

scholarly journals Internucleosomal DNA cleavage and neuronal cell survival/death

1993 ◽  
Vol 122 (3) ◽  
pp. 523-532 ◽  
Author(s):  
A Batistatou ◽  
LA Greene
Keyword(s):  
Cell Death ◽  
Cell Survival ◽  
Pc12 Cells ◽  
Dna Fragmentation ◽  
Cell Cultures ◽  
Pc12 Cell ◽  
Dna Cleavage ◽  
Sympathetic Neurons ◽  
Term Survival ◽  
Serum Withdrawal

Serum-free PC12 cell cultures have been used to study the mechanisms of neuronal death after neurotrophic factor deprivation. We previously reported that PC12 cells undergo "apoptotic" internucleosomal DNA cleavage after withdrawal of trophic support. Here, we have used a sensitive method to detect PC12 cell DNA fragmentation within three hrs of serum removal and have exploited this assay to examine several aspects regarding the mechanisms of neuronal survival/death. Major advantages of this assay are that it permits acute experiments to be performed well before other manifest signs of cell death and under conditions that cannot be applied chronically. We find that this apopotic DNA fragmentation is distinct from the random DNA degradation that occurs during necrotic death. Major observations include the following: (a) There is a good correlation between the ability of trophic substances to promote PC12 cell survival and to inhibit early DNA fragmentation. (b) Phorbol ester, an activator of PKC, acutely suppresses DNA fragmentation, but does not promote long-term survival or inhibition of endonuclease activity when applied chronically due to its downregulation of PKC. (c) Cells undergoing apoptosis within 3 h of serum withdrawal have a "commitment point" of only 1.0-1.5 h beyond which they can no longer be rescued by NGF. (d) Aurin, a non-carboxylic analog of the endonuclease inhibitor ATA, also inhibits DNA fragmentation and promotes short-term survival of PC12 cells. (e) Macromolecular synthesis is not required for DNA fragmentation or for NGF to prevent this event. (f) Extracellular Ca2+ is not required for internucleosomal DNA cleavage caused by serum withdrawal or for suppression of this by NGF. (g) DNA fragmentation can also be detected in cultures of rat sympathetic neurons as early as 10 h after removal of NGF. As in PC12 cell cultures, this precedes morphological signs of cell death.

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