Hypoxia and P1 receptor activation regulate the high-affinity concentrative adenosine transporter CNT2 in differentiated neuronal PC12 cells

2013 ◽  
Vol 454 (3) ◽  
pp. 437-445 ◽  
Author(s):  
Lorena Medina-Pulido ◽  
Míriam Molina-Arcas ◽  
Carles Justicia ◽  
Eduardo Soriano ◽  
Ferran Burgaya ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Receptor Activation ◽  
Nucleoside Transporter ◽  
Concentrative Nucleoside Transporter ◽  
Adenosine Uptake ◽  
P1 Receptor ◽  
Cell Energy ◽  
Neuronal Pc12 Cells ◽  
Amp Activated Protein Kinase ◽  
Kinase Phosphorylation

Neuronal PC12 cells express the adenosine CNT2 (concentrative nucleoside transporter 2), which is regulated by purinergic P1 receptors and hypoxia/ischaemia. CNT2-dependent adenosine uptake promotes AMPK (AMP-activated protein kinase) phosphorylation. CNT2 may modulate extracellular adenosine and cell energy balance in neuronal tissue.

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.

scholarly journals Decreased Equilibrative Nucleoside Transporter 1 (ENT1) Activity Contributes to the High Extracellular Adenosine Levels in Mesenchymal Glioblastoma Stem-Like Cells

Cells ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 1914 ◽  
Author(s):  
Sebastián Alarcón ◽  
María de los Ángeles Toro ◽  
Carolina Villarreal ◽  
Rómulo Melo ◽  
Rodrigo Fernández ◽  
...  
Keyword(s):  
Adenosine Monophosphate ◽  
Prostatic Acid Phosphatase ◽  
Cell Subpopulation ◽  
Migration And Invasion ◽  
Nucleoside Transporter ◽  
Extracellular Adenosine ◽  
Adenosine Uptake ◽  
A Cell ◽  
High Level ◽  
Lower Expression

Glioblastoma multiforme is one of the most malignant types of cancer. This is mainly due to a cell subpopulation with an extremely aggressive potential, called glioblastoma stem-like cells (GSCs). These cells produce high levels of extracellular adenosine which has been associated with increased chemoresistance, migration, and invasion in glioblastoma. In this study, we attempted to elucidate the mechanisms that control extracellular adenosine levels in GSC subtypes. By using primary and U87MG-derived GSCs, we associated increased extracellular adenosine with the mesenchymal phenotype. [3H]-adenosine uptake occurred mainly through the equilibrative nucleoside transporters (ENTs) in GSCs, but mesenchymal GSCs have lower expression and ENT1-mediated uptake activity than proneural GSCs. By analyzing expression and enzymatic activity, we determined that ecto-5′-nucleotidase (CD73) is predominantly expressed in proneural GSCs, driving AMPase activity. While in mesenchymal GSCs, both CD73 and Prostatic Acid Phosphatase (PAP) contribute to the AMP (adenosine monophosphate) hydrolysis. We did not observe significant differences between the expression of proteins involved in the metabolization of adenosine among the GCSs subtypes. In conclusion, the lower expression and activity of the ENT1 transporter in mesenchymal GSCs contributes to the high level of extracellular adenosine that these GSCs present.

scholarly journals Conserved Glutamate Residues Glu-343 and Glu-519 Provide Mechanistic Insights into Cation/Nucleoside Cotransport by Human Concentrative Nucleoside Transporter hCNT3

2009 ◽  
Vol 284 (25) ◽  
pp. 17266-17280 ◽  
Author(s):  
Melissa D. Slugoski ◽  
Kyla M. Smith ◽  
Amy M. L. Ng ◽  
Sylvia Y. M. Yao ◽  
Edward Karpinski ◽  
...  
Keyword(s):  
Nucleoside Transporter ◽  
Concentrative Nucleoside Transporter
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