| Title | Combined treatment of aspartyl protease inhibitor and Nmda antagonist in Pc12 cells after glutamate excitotoxicity | ||
| Authors | C. Pourzitaki1, G. Kanellos2, I. Klagas1 and A. Kritis2
1. Laboratory of Pharmacology and 2. Laboratory of Physiology, School of Medicine, Aristotle University of Thessaloniki, Greece |
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| Citation | Pouritzaki, C., Kanellos, G., Klagas, I., Kritis, A.: Combined treatment of aspartyl protease inhibitor and Nmda antagonist in Pc12 cells after glutamate excitotoxicity, Epitheorese Klin. Farmakol. Farmakokinet. 22(2): 304-307 (2008) | ||
| Publication Date | 23-25 May 2008 | ||
| Full Text Language | English | ||
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| Keywords | Cell death, Glutamate, Toxicity, PC12, NGF, Pepstatin A, MK801. | ||
| Other Terms | Review article | ||
| Summary | Unrestrained calcium influx can trigger potentially lethal biochemical pathways that involve degradative enzymes (e.g. proteases and endonucleases) and increased synthesis of oxygen free radicals which injure and damage neurons. Such mechanisms are implicated in acute and chronic neurodegenerative diseases. In the present study we investigated the molecular response of central nervous system to glutamate induced exitotoxicity using PC12 cell cultures. These chromaffinergic transformed cells upon treatment with nerve growth factor (NGF), differentiate to a sympathetic phenotype expressing neurites and excitability. PC12 cells were cultured in full medium DMEM at 37ºC with 5% CO2. Glutamate excitotoxicity was induced by exposing undifferentiated and NGF-treated PC12 cultures to two different glutamate concentrations (0,5 μM and 10 μΜ), for 3h. We investigated the involvement of aspartyl proteases and NMDA receptor antagonists in cell death induced by glutamate toxicity, using an aspartyl-protease inhibitor Pepstatin A and a potent NMDA receptor antagonist MK801. Cell viability was estimated by a colorimetric method using MTT [3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyl tetrazolium bromide. We found that Pepstatin A protects cells from death induced by low glutamate concentrations of both naive and NGF treated cells. However at high glutamate concentrations only combined treatment rescues cells from excitotoxic death. | ||
| References | 1. Greene L.A., Aletta J.M., Rukenstein A., Green S.H.: PC12 pheochromocytoma cells: culture, nerve growth factor treatment, and experimental exploitation. Methods Enzymol. 147: 207-216 (1987)
2. Choi D.W., Hartley D.M.: Calcium and glutamate-induced cortical neuronal death, In: (S.G. Waxman, ed.) Molecular and Cellular Approaches to the Treatment of Neurological Disease. Pp. 23-34, Raven Press, New York, 1993 3. Hossmann K.A.: Glutamate-mediated injury in focal cerebral ischemia: the excitotoxin hypothesis revised. Brain Pathol. 4: 23-36 (1994) 4. Choi D.W.: Glutamate neurotoxicity and diseases of the nervous system. Trends Neurosci. 11: 465-469 (1988) 5. Vaux D.L., Korsmeyer S.J.: Cell death in development. Cell 96: 245-254 (1999) |
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| Relative Papers | |||
Online ISSN 1011-6575
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Articles published in this Journal are Indexed or Abstracted in: • Chemical Abstracts • Elsevier’s Bibliographic Databases: Scopus, EMBASE, EMBiology, Elsevier BIOBASE SCImago Journal and Country Rank Factor
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