ArticleNeurochemical research2004
Decreased copper-zinc superoxide dismutase activity and increased resistance to oxidative stress in glia maturation factor-null astrocytes.
Article in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Glial maturation factor-β deficiency prevents oestrogen deficiency-induced bone loss by remodelling the actin network to suppress adipogenesis of bone marrow mesenchymal stem cells.Cell death & disease · 2024Article
- Molecular Association of Glia Maturation Factor with the Autophagic Machinery in Rat Dopaminergic Neurons: a Role for Endoplasmic Reticulum Stress and MAPK Activation.Molecular neurobiology · 2019Article
- Brain-Derived Glia Maturation Factor β Participates in Lung Injury Induced by Acute Cerebral Ischemia by Increasing ROS in Endothelial Cells.Neuroscience bulletin · 2018Article
- Glia Maturation Factor Dependent Inhibition of Mitochondrial PGC-1α Triggers Oxidative Stress-Mediated Apoptosis in N27 Rat Dopaminergic Neuronal Cells.Molecular neurobiology · 2018Article
- Glia maturation factor-β: a potential therapeutic target in neurodegeneration and neuroinflammation.Neuropsychiatric disease and treatment · 2018Review
- First description of enhanced expression of glia maturation factor-beta in experimental toxoplasmic encephalitis.The Journal of international medical research · 2017Article
- Article
- Suppression of glia maturation factor expression prevents 1-methyl-4-phenylpyridinium (MPP⁺)-induced loss of mesencephalic dopaminergic neurons.Neuroscience · 2014Article
- Glia maturation factor deficiency suppresses 1-methyl-4-phenylpyridinium-induced oxidative stress in astrocytes.Journal of molecular neuroscience : MN · 2014Article
- Neurotrophic Signaling Factors in Brain Ischemia/Reperfusion Rats: Differential Modulation Pattern between Single-Time and Multiple Electroacupuncture Stimulation.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- Clinical course of myelin oligodendrocyte glycoprotein 35-55 induced experimental autoimmune encephalomyelitis is aggravated by glia maturation factor.Neurochemistry international · 2012Article
- Contribution of mitochondrial network dynamics to intracellular ROS signaling.Communicative & integrative biology · 2012Article
- Augmented expression of glia maturation factor in Alzheimer's disease.Neuroscience · 2011Article
- Suppression of neuro inflammation in experimental autoimmune encephalomyelitis by glia maturation factor antibody.Brain research · 2011Article
- Article
- Overexpression of glia maturation factor reinstates susceptibility to myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis in glia maturation factor deficient mice.Neurobiology of disease · 2010Article
- Allostatic tumor-burden induces depression-associated changes in hepatoma-bearing mice.Journal of neuro-oncology · 2009Article
- Glutamate transporter EAAT2 expression is up-regulated in reactive astrocytes in human periventricular leukomalacia.The Journal of comparative neurology · 2008Article
- Glia maturation factor regulation of STAT expression: a novel mechanism in experimental autoimmune encephalomyelitis.Neurochemical research · 2007Article
- Diminished cytokine and chemokine expression in the central nervous system of GMF-deficient mice with experimental autoimmune encephalomyelitis.Brain research · 2007Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Glia maturation factor (GMF) is a highly conserved protein found mainly in the nervous system. The current work was undertaken to investigate the effect of GMF expression in astrocytes on CuZn superoxide dismutase (CuZnSOD or SOD I) and on the vulnerability of the cells to H2O2 toxicity. Primary astrocyte cultures were derived from mice in which the GMF gene was completely deleted by homologous recombination (knockout). Astocytes derived from knockout animals displayed a lower level of CuZnSOD activity and protein. The reduction in CuZnSOD was restored by transfection with a GMF/adenovirus construct, and the resulting increase was blocked by the p38 MAP kinase inhibitor SB203580. There was no change in the other isoform of SOD (MnSOD or SOD II). Endogenous H2O2 was lower in the knockout cells, and the cells became more resistant to H2O2 toxicity compared to the wild type. In the GMF-null cells, concurrent with a decrease in CuZnSOD, the function of which is to convert superoxide to H2O2, there was an increase in the activity of the two enzymes that degrade H2O2: catalase and glutathione peroxidase. By regulating the redox state of the cell, GMF may be involved in a wide spectrum of cellular events ranging from survival, proliferation, differentiation, to death.
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