| Involvement of Hsp70, a stress protein, in the resistance of long-term culture of PC12 cells against sodium nitroprusside (SNP)-induced cell death. | |
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MedLine Citation:
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PMID: 20559625 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Sodium nitroprusside (SNP)-treated PC12 cell line is being used in our laboratory as a cell model of nitric oxide (NO)-mediated damage for in vitro evaluation of potential neuroprotective compounds, thus cell response to SNP must be standardized to gain reproducible data. The NO-donor SNP has been shown to induce cell death at high concentrations in undifferentiated PC12 cells. Differences were found in sensitivity to SNP between cells from short- and long-term cultured cells. After 24-h exposure to 100-500 microM SNP, a decrease of cell viability was observed in both short- (17, 21 and 23rd passages) and long-term cultures (46, 49 and 50th passages), with IC(50) values of 312.72 and 462.90 microM, respectively. In cells from early passages, SNP-induced cell death was accompanied by significant increases of LDH leakage, nitrite production, malondialdehyde (MDA) levels, catalase (CAT) activity, cleavage of poly(ADP-ribose)polymerase (PARP) and caspase-3 activation in comparison with those from late passages. Furthermore, untreated and SNP-treated cells from long-term cultures displayed an increase of the stress protein Hsp70 levels when compared with those from short-term cultures. Up-regulated levels of Hsp70 may be associated with cell survival. Therefore, cells may acquire a certain resistance to SNP-induced toxicity associated with an increase in cell passage-dependent Hsp70. The protein Hsp70 might modulate the cellular response to the toxic insult by increasing CAT and GSH-Px activities and decreasing caspase-3 activation. Finally, it is crucial for the standardization of this cell model of neurotoxicity, at least in part, the use of PC12 cells in an optimum and reliable range of passages. |
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Authors:
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Carmen Romero; Juana Benedí; Angel Villar; Sagrario Martín-Aragón |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-06-18 |
Journal Detail:
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Title: Archives of toxicology Volume: 84 ISSN: 1432-0738 ISO Abbreviation: Arch. Toxicol. Publication Date: 2010 Sep |
Date Detail:
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Created Date: 2010-09-02 Completed Date: 2010-12-02 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0417615 Medline TA: Arch Toxicol Country: Germany |
Other Details:
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Languages: eng Pagination: 699-708 Citation Subset: IM |
Affiliation:
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Pharmacology Department, School of Pharmacy, Complutense University of Madrid, 28040 Madrid, Spain. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis Caspase 3 / metabolism Cell Culture Techniques Cell Death Cell Survival HSP70 Heat-Shock Proteins / metabolism*, pharmacology Neuroprotective Agents / toxicity* Nitric Oxide / metabolism, toxicity* Nitric Oxide Donors / toxicity Nitroprusside / toxicity* PC12 Cells Poly(ADP-ribose) Polymerases / metabolism Rats |
| Chemical | |
Reg. No./Substance:
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0/HSP70 Heat-Shock Proteins; 0/Neuroprotective Agents; 0/Nitric Oxide Donors; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 3.4.22.-/Caspase 3 |
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