Induction of Apoptosis and Activation of JNK and p38 MAPK Pathways in Deoxynivalenol-Treated Cell Lines
| Autor: | Daiva Baltriukiene, Virginija Bukelskiene, Audrone Kalvelyte |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Programmed cell death
Cell Survival p38 mitogen-activated protein kinases Immunoblotting Apoptosis DNA Fragmentation Toxicology p38 Mitogen-Activated Protein Kinases Jurkat cells General Biochemistry Genetics and Molecular Biology Jurkat Cells Mice Cricetinae Animals Humans Dose-Response Relationship Drug biology Cell growth Kinase c-jun JNK Mitogen-Activated Protein Kinases General Medicine Cell biology Enzyme Activation Medical Laboratory Technology Biochemistry Mitogen-activated protein kinase biology.protein Signal transduction Trichothecenes Signal Transduction |
| Zdroj: | Alternatives to Laboratory Animals. 35:53-59 |
| ISSN: | 2632-3559 0261-1929 |
| DOI: | 10.1177/026119290703500101 |
| Popis: | Deoxynivalenol (DON) is a mycotoxin produced by what are thought to be the most prevalent toxin-producing fungi of the Fusarium genus. Here, we present the results of apoptosis induction, phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinases (MAPKs), and expression of the c-Jun protein after DON treatment, in a pre-B lymphocyte REH cell line. In addition, human pre-T lymphocyte Jurkat, hamster kidney-derived BHK21 and mouse hepatoma MH-22a cells were used in comparative experiments in vitro. We found that the DON effect was cell origin-dependent and dose-dependent, with a significant slow-down of cell proliferation and increase of apoptotic cells in blood cell lines. BHK21 and MH-22a cells were less sensitive to the DON effect. In blood-derived REH and Jurkat cells, DON-induced apoptotic changes were preceded by an increase in JNK and p38 MAPKs phosphorylation, as well as in c-Jun expression. However, the activation of JNK phosphorylation and c-Jun expression were transient, but did not coincide with each other. An inhibitor of JNK1/2, SP600125, had a negligible negative effect on REH cell viability after DON treatment, demonstrating that JNK does not contribute to DON-induced apoptosis. In contrast, studies on the role of p38 MAPK revealed that p38 signalling is required for DON-induced apoptosis in REH cells. |
| Databáze: | OpenAIRE |
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