Importance of mitochondrial dysfunction in oxidative stress response: A comparative study of gene expression profiles
| Autor: | Tetsu Uchida, Kazunori Mori, Fumihiro Ishikawa, Kyota Ushida, Motoko Shibanuma, Anna Inoue, Kiyoshi Nose |
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| Rok vydání: | 2011 |
| Předmět: |
Transcription
Genetic Matrix metalloproteinase Biology medicine.disease_cause Biochemistry Cell Line Electron Transport Complex IV Electron Transport Complex III Mice Prohibitins Gene expression medicine Animals Oligonucleotide Array Sequence Analysis Membrane Potential Mitochondrial chemistry.chemical_classification Regulation of gene expression Reactive oxygen species Superoxide Dismutase Gene Expression Profiling Cytochromes c NADH Dehydrogenase Hydrogen Peroxide General Medicine Matrix Metalloproteinases Mitochondria Cell biology Repressor Proteins Succinate Dehydrogenase Gene expression profiling Oxidative Stress Gene Expression Regulation chemistry Cell culture Coenzyme Q – cytochrome c reductase Oxidative stress |
| Zdroj: | Free Radical Research. 45:672-680 |
| ISSN: | 1029-2470 1071-5762 |
| DOI: | 10.3109/10715762.2011.564169 |
| Popis: | Mitochondria are considered to play an important role in oxidative stress response since they are a source of reactive oxygen species and are also targeted by these species. This study examined the mitochondrial conditions in cells of epithelial origin that were exposed to H(2)O(2) and found a decline in the membrane potential along with a specific loss of UQCRC1, a sub-unit of complex III, suggesting that mitochondrial dysfunction occurs upon exposure to oxidative stress. This observation led to the hypothesis that certain cellular responses to oxidative stress occurred because of mitochondrial dysfunction. When mitochondria-less (pseudo ρ0) cells were examined as a model of mitochondrial dysfunction, striking similarities were found in their cellular responses compared with those found in cells exposed to oxidative stress, including changes in gene expression and gelatinolytic enzyme activities, thus suggesting that cellular responses to oxidative stress were partly mediated by mitochondrial dysfunction. This possibility was further validated by microarray analysis, which suggested that almost one-fourth of the cellular responses to oxidative stress were mediated by mitochondrial dysfunction that accompanies oxidative stress, thereby warranting a therapeutic strategy that targets mitochondria for the treatment of oxidative stress-associated diseases. |
| Databáze: | OpenAIRE |
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