Salidroside fromRhodiola sachalinensisProtects Neuronal PC12 Cells Against Cytotoxicity Induced by Amyloid‐β

2003 ◽  
Vol 25 (3) ◽  
pp. 295-304 ◽  
Author(s):  
S. I. Jang ◽  
H. O. Pae ◽  
B. M. Choi ◽  
G. S. Oh ◽  
S. Jeong ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Amyloid Β ◽  
Neuronal Pc12 Cells

Designed Short Peptides that Form Amyloid-Like Fibrils in Coassembly with Amyloid β-Peptide (Aβ) Decrease the Toxicity of Aβ to Neuronal PC12 Cells

ChemBioChem ◽  
2010 ◽  
Vol 11 (11) ◽  
pp. 1525-1530 ◽  
Author(s):  
Miho Suzuki ◽  
Tsuyoshi Takahashi ◽  
Junichi Sato ◽  
Masayasu Mie ◽  
Eiry Kobatake ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Amyloid Β ◽  
Short Peptides ◽  
Amyloid Β Peptide ◽  
Neuronal Pc12 Cells

scholarly journals Cover Picture: Designed Short Peptides that Form Amyloid-Like Fibrils in Coassembly with Amyloid β-Peptide (Aβ) Decrease the Toxicity of Aβ to Neuronal PC12 Cells (ChemBioChem 11/2010)

ChemBioChem ◽  
2010 ◽  
Vol 11 (11) ◽  
pp. 1473-1473
Author(s):  
Miho Suzuki ◽  
Tsuyoshi Takahashi ◽  
Junichi Sato ◽  
Masayasu Mie ◽  
Eiry Kobatake ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Amyloid Β ◽  
Short Peptides ◽  
Amyloid Β Peptide ◽  
Neuronal Pc12 Cells

scholarly journals Sesamin Modulates Tyrosine Hydroxylase, Superoxide Dismutase, Catalase, Inducible No Synthase and Interleukin-6 Expression in Dopaminergic Cells Under Mpp+-Induced Oxidative Stress

2008 ◽  
Vol 1 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Vicky Lahaie-Collins ◽  
Julie Bournival ◽  
Marilyn Plouffe ◽  
Julie Carange ◽  
Maria-Grazia Martinoli
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Tyrosine Hydroxylase ◽  
Protein Expression ◽  
Pc12 Cells ◽  
Interleukin 6 ◽  
Estrogen Receptor Alpha ◽  
Strong Increase ◽  
Mrna Levels ◽  
Neuronal Pc12 Cells

Oxidative stress is regarded as a mediator of nerve cell death in several neurodegenerative disorders, such as Parkinson's disease. Sesamin, a lignan mainly found in sesame oil, is currently under study for its anti-oxidative and possible neuroprotective properties. We used 1-methyl-4-phenyl-pyridine (MPP+) ion, the active metabolite of the potent parkinsonism-causing toxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine, to produce oxidative stress and neurodegeneration in neuronal PC12 cells, which express dopamine, as well as neurofilaments. Our results show that picomolar doses of sesamin protected neuronal PC12 cells from MPP+-induced cellular death, as revealed by colorimetric measurements and production of reactive oxygen species. We also demonstrated that sesamin acted by rescuing tyrosine hydroxylase levels from MPP+-induced depletion. Sesamin, however, did not modulate dopamine transporter levels, and estrogen receptor-alpha and -beta protein expression. By examining several parameters of cell distress, we found that sesamin also elicited a strong increase in superoxide dismutase activity as well as protein expression and decreased catalase activity and the MPP+stimulated inducible nitric oxide synthase protein expression, in neuronal PC12 cells. Finally, sesamin possessed significant anti-inflammatory properties, as disclosed by its potential to reduce MPP+-induced interleukin-6 mRNA levels in microglia. From these studies, we determined the importance of the lignan sesamin as a neuroprotective molecule and its possible role in complementary and/or preventive therapies of neurodegenerative diseases.

scholarly journals The dynamic pattern of glucocorticoid receptor-mediated transcriptional responses in neuronal PC12 cells

2006 ◽  
Vol 99 (4) ◽  
pp. 1282-1298 ◽  
Author(s):  
M. C. Morsink ◽  
M. Joëls ◽  
R. A. Sarabdjitsingh ◽  
O. C. Meijer ◽  
E. R. De Kloet ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Pc12 Cells ◽  
Transcriptional Responses ◽  
Dynamic Pattern ◽  
Neuronal Pc12 Cells

Effect of Neuronal PC12 Cells on the Functional Properties of Intestinal Epithelial Caco-2 Cells

2003 ◽  
Vol 67 (6) ◽  
pp. 1312-1318 ◽  
Author(s):  
Hideo SATSU ◽  
Tatsuya YOKOYAMA ◽  
Nobumasa OGAWA ◽  
Yoko FUJIWARA-HATANO ◽  
Makoto SHIMIZU
Keyword(s):  
Pc12 Cells ◽  
Functional Properties ◽  
Intestinal Epithelial ◽  
Neuronal 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.

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