Nitric oxide mediated induction of cytochrome c oxidase mRNA and protein in a mouse macrophage cell line
| Autor: | Bonnie L. Firestein, David S. Bredt, Joshua E. Lehrer-Graiwer |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Oxidative phosphorylation
Mitochondrion Nitric Oxide Cell Line Nitric oxide Electron Transport Complex IV Mice chemistry.chemical_compound Western blot medicine Animals Cytochrome c oxidase RNA Messenger chemistry.chemical_classification biology medicine.diagnostic_test Macrophages General Neuroscience Neurotoxicity Nucleic Acid Hybridization medicine.disease Molecular biology Up-Regulation Enzyme chemistry Biochemistry Apoptosis Enzyme Induction biology.protein |
| Zdroj: | Neuroscience Letters. 288:107-110 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/s0304-3940(00)01205-2 |
| Popis: | Neurons that express neuronal nitric oxide synthase (nNOS) are selectively spared from nitric oxide (NO)-induced cytotoxicity in acute cerebral ischemia and neurodegenerative conditions but the mechanism of this resistance is unknown. To identify specific gene products which may mediate this resistance, we performed polymerase chain reaction (PCR)-based subtractive hybridization on a mouse macrophage cell line treated with either L-NG-nitroarginine methyl ester (L-NAME, 1 mM, 1 h), an inhibitor of NOS, or with diethylamine NONOate (DEA NONO, 200 microM, 1 h), an NO donor. NO-treated cultures showed an acute induction of mRNA (less than 1 h after treatment) and protein (15 min) for the mitochondrial enzyme cytochrome c oxidase (CcO) as shown by Northern or Western blot analysis, respectively. Cytochrome c oxidase activity assay showed constant activity in NO-treated cultures, as compared to L-NAME-treated cultures. NO directly inhibits CcO, the terminal electron acceptor in mitochondrial oxidative respiration. Up-regulation of this enzyme by NO, therefore, appears to maintain vital CcO activity and cellular energy stores, thus contributing to selective sparing of nNOS neurons. |
| Databáze: | OpenAIRE |
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