Proteomic analysis of mitochondrial proteins of basal and lipolytically (isoproterenol and TNF-α)-stimulated adipocytes
| Autor: | Jung Ho Lee, Pil Joon Park, Hui Kyoung Chang, Tae Ryong Lee, Eui Seok Shin, Si Young Cho |
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| Rok vydání: | 2009 |
| Předmět: |
Proteomics
Protein Folding medicine.medical_specialty Oxidative phosphorylation Biology Mitochondrion medicine.disease_cause Biochemistry Cell Line Proinflammatory cytokine Mitochondrial Proteins Mice chemistry.chemical_compound Adenosine Triphosphate Internal medicine Adipocyte Adipocytes medicine Animals Electrophoresis Gel Two-Dimensional Phosphorylation Prohibitin Molecular Biology Beta oxidation Tumor Necrosis Factor-alpha Fatty Acids Isoproterenol Cell Biology Lipid Metabolism Citric acid cycle Endocrinology chemistry Oxidation-Reduction Oxidative stress |
| Zdroj: | Journal of Cellular Biochemistry. 106:257-266 |
| ISSN: | 1097-4644 0730-2312 |
| DOI: | 10.1002/jcb.21998 |
| Popis: | The regulation of adipocyte lipolysis is increasingly believed to influence insulin resistance, in a process that may be associated with mitochondrial dysfunction. However, the molecular basis of the relationship between mitochondrial protein expression, lipolytic responsiveness, and insulin resistance remains unknown. A set of proteins that shows altered abundances in the mitochondria of untreated and treated 3T3-L1 adipocytes with TNF-alpha or isoproterenol was identified. These include the proteins associated with energy production, including fatty acid oxidation, TCA cycle, and oxidative phosphorylation. Proteins associated with oxidative stress dissipation were down-regulated in lipolytically stimulated adipocytes. Lipolytic stimulation with isoproterenol and TNF-alpha, which is also a potent proinflammatory cytokine, showed some noticeable differences in mitochondrial protein expression. For example, isoproterenol markedly enhanced the expression of prohibitin which is involved in the integrity of mitochondria but TNF-alpha did not. These results provide valuable information on mitochondrial dysfunction associated with oxidative stress induced by lipolytic stimulation. |
| Databáze: | OpenAIRE |
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