Enhanced neuronal protection from oxidative stress by coculture with glutamic acid decarboxylase‐expressing astrocytes
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Astrocytes expressing glutamic acid decarboxylase GAD67 directed by the glial fibrillary acidic protein promoter were shown to provide enhanced protection of PC12 cells from H 2 O 2 treatment and serum deprivation in the presence of glutamate. In addition, they protected non‐differentiated, but not differentiated, embryonic rat cortical neurons from glutamate toxicity. Glutamic acid decarboxylase (GAD)‐expressing astrocytes showed increased glutathione synthesis and release compared to control astrocytes. These changes were due to GAD transgene expression, as transient expression of a GAD antisense plasmid resulted in partial suppression of the increase in glutathione release. In addition to the previously demonstrated increases in NADH and ATP levels and lactate release, GAD‐expressing astrocytes show increased antioxidant activity, explaining their ability to protect neurons from various injuries.
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Several reports showed that enhanced GAD2 activity may contribute to neuronal protection from oxidative stress in vitro neuronal tissue cultures.
“In this way, several reports showed that enhanced GAD2 activity may contribute to neuronal protection from oxidative stress in vitro neuronal tissue cultures [238, 239].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [239]
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Balmus, I. M., Ciobica, A., Antioch, I., Dobrin, R., & Timofte, D. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/3975101 · Cited by 103 · see citing works
“In this way, several reports showed that enhanced GAD2 activity may contribute to neuronal protection from oxidative stress in vitro neuronal tissue cultures [238, 239].”
BackgroundLamigeon, C., Prod'Hon, C., De Frias, V, Michoudet, C., & Jacquemont, B. (2003) · Experimental Neurology · doi:10.1016/s0014-4886(03)00400-x · Cited by 13 · see citing works
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- Authors
- Lamigeon, C., Bellier, J. P., Sacchettoni, S., Rujano, M., & Jacquemont, B.
- Affiliations
- Inserm (FR)
- Hospital Vargas (VE)
- Corresponding author
- Jacquemont, B.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2001-04-15
- Volume
- 77
- Issue
- 2
- Pages
- 598-606
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1544500316
- Cited by
- 41
- References
- 69
- Citations by year
- 2024: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2016: 4 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 5
- FWCI
- 0.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Keywords
- glutamic acid decarboxylase, GAD67, astrocytes, neuroprotection, oxidative stress, glutamate excitotoxicity, hydrogen peroxide, serum deprivation, PC12 cells, glutathione synthesis, glutathione release, antioxidant activity, glial fibrillary acidic protein promoter, lactate release, NADH, ATP, cortical neurons
- MeSH terms
- Animals, Astrocytes, Cell Differentiation, Energy Metabolism, Genes, Synthetic, Glial Fibrillary Acidic Protein, Glutamate Decarboxylase, Glutathione, Hydrogen Peroxide, Isoenzymes, Neoplasm Proteins, Nerve Tissue Proteins, Neurons, Oxidation-Reduction, Promoter Regions, Genetic, Recombinant Fusion Proteins, Transfection, PC12 Cells, Culture Media, Serum-Free, Oxidative Stress, Glutamic Acid, Coculture Techniques, Transgenes, Mice, Rats
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