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Your search keyword '"metabolism, Oxidation-Reduction, Oxidative Stress"' showing total 2 results
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2 results on '"metabolism, Oxidation-Reduction, Oxidative Stress"'

1. Increased resistance to oxidative DNA damage of trabecular meshwork cells byE. coli FPGgene transfection

Author

Mara Foresta, Alberto Izzotti, Sergio Claudio Saccà, Mariagrazia Longobardi, Cristina Cartiglia, and Guido Frosina

Subjects
DNA repair, Recombinant Fusion Proteins, genetics/metabolism, Gene Expression, biosynthesis/genetics, Biology, Transfection, medicine.disease_cause, Biochemistry, Cell Line, chemistry.chemical_compound, Trabecular Meshwork, Cell Line, Tumor, Escherichia coli, medicine, Humans, genetics, analogs /&/ derivatives/analysis, Tumor, DNA Damage, DNA-Formamidopyrimidine Glycosylase, genetics, Deoxyguanosine, analogs /&/ derivatives/analysis, Endothelial Cells, metabolism, Escherichia coli Proteins, genetics, Escherichia coli, genetics/metabolism, Gene Expression, Gene Therapy, Glaucoma, genetics/prevention /&/ control/therapy, Humans, Mitochondria, metabolism, Oxidation-Reduction, Oxidative Stress, genetics, Reactive Oxygen Species, metabolism, Recombinant Fusion Proteins, biosynthesis/genetics, Trabecular Meshwork, cytology/metabolism, Transfection, cytology/metabolism, chemistry.chemical_classification, Reactive oxygen species, Tumor, Escherichia coli Proteins, genetics/prevention /&/ control/therapy, Deoxyguanosine, Endothelial Cells, Glaucoma, Gene Therapy, Genetic Therapy, General Medicine, Formamidopyrimidine DNA glycosylase, Molecular biology, Mitochondria, Oxidative Stress, medicine.anatomical_structure, DNA-Formamidopyrimidine Glycosylase, chemistry, 8-Hydroxy-2'-Deoxyguanosine, DNA glycosylase, Trabecular meshwork, Reactive Oxygen Species, metabolism, Oxidation-Reduction, DNA, DNA Damage
Abstract

Oxidative damage plays a pathogenic role in various chronic degenerative diseases. Oxidative damage targeting trabecular meshwork (TM) cells as a consequence of mitochondrial damage is a pathogenic mechanism for glaucoma, the most common cause of irreversible blindness worldwide. Consequences of oxidative damage are attenuated by endocellular activities involved in scavenging reactive oxidative species and DNA repair. Selected bacterial genes are highly efficient at protecting cells from oxidative DNA damage. This situation occurs for Escherichia coli formamidopyrimidine DNA glycosylase (FPG), a major DNA glycosylase that repairs oxidatively damaged DNA. Accordingly, this study was aimed at transfecting human TM cells (HTMC) with Fpg in order to increase their resistance to oxidative damage. This study demonstrates that it is feasible to increase resistance of HTMC to endogenous oxidative damage by gene transfection. These findings bear relevance for primary and secondary prevention of degenerative glaucomas and other degenerative diseases where oxidative damage plays a pathogenic role.

Published
2011

2. SUMO: a (oxidative) stressed protein

Author

Robert Nisticò and Marco Feligioni

Subjects
Protein sumoylation, MAP Kinase Signaling System, SUMO protein, Nerve Tissue Proteins, Oxidative phosphorylation, medicine.disease_cause, Animals, Diabetes Mellitus, Humans, JNK Mitogen-Activated Protein Kinases, Neoplasm Proteins, Neoplasms, Neurodegenerative Diseases, Oxidation-Reduction, Oxidative Stress, Reactive Oxygen Species, Signal Transduction, Small Ubiquitin-Related Modifier Proteins, Sumoylation, Ubiquitin, Ubiquitin-Protein Ligase Complexes, Cellular and Molecular Neuroscience, medicine, biology, phy/siology, Neurodegeneration, Settore BIO/14, medicine.disease, Sumoylation Pathway, Cell biology, Animals, Diabetes Mellitus, metabolism, Humans, JNK Mitogen-Activated Protein Kinases, physiology, MAP Kinase Signaling System, physiology, Neoplasm Proteins, metabolism, Neoplasms, metabolism, Nerve Tissue Proteins, metabolism, Neurodegenerative Diseases, metabolism, Oxidation-Reduction, Oxidative Stress, physiology, Reactive Oxygen Species, metabolism, Signal Transduction, Small Ubiquitin-Related Modifier Proteins, physiology, Sumoylation, physiology, Ubiquitin, physiology, Ubiquitin-Protein Ligase Complexes, Neurology, Biochemistry, physiology, biology.protein, Molecular Medicine, Signal transduction, metabolism, Oxidative stress
Abstract

Redox species are produced during the physiological cellular metabolism of a normal tissue. In turn, their presence is also attributed to pathological conditions including neurodegenerative diseases. Many are the molecular changes that occur during the unbalance of the redox homeostasis. Interestingly, posttranslational protein modifications (PTMs) play a remarkable role. In fact, several target proteins are modified in their activation, localization, aggregation, and expression after the cellular stress. Among PTMs, protein SUMOylation represents a very important molecular modification pathway during “oxidative stress”. It has been reported that this ubiquitin-like modification is a fine sensor for redox species. Indeed, SUMOylation pathway efficiency is affected by the exposure to oxidative species in a different manner depending on the concentration and time of application. Thus, we here report updated evidence that states the role of SUMOylation in several pathological conditions, and we also outline the key involvement of c-Jun N-terminal kinase and small ubiquitin modifier pathway cross talk.

Published
2013

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