ArticleThe Journal of biological chemistry2010
Neurons efficiently repair glutamate-induced oxidative DNA damage by a process involving CREB-mediated up-regulation of apurinic endonuclease 1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 92 citations in OpenAlex.
- Safeguarding genomic integrity in beta-cells: implications for beta-cell differentiation, growth, and dysfunction.Biochemical Society transactions · 2024Review
- The role of aging and brain-derived neurotrophic factor signaling in expression of base excision repair genes in the human brain.Aging cell · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- The neuroprotective effects of glucagon-like peptide 1 in Alzheimer's and Parkinson's disease: An in-depth review.Frontiers in neuroscience · 2022Review
- The Role of DNA Damage in Neural Plasticity in Physiology and Neurodegeneration.Frontiers in cellular neuroscience · 2022Review
- Neuroprotective Mechanisms of Glucagon-Like Peptide-1-Based Therapies in Ischemic Stroke: An Update Based on Preclinical Research.Frontiers in neurology · 2022Review
- In Pursuit of Healthy Aging: Effects of Nutrition on Brain Function.International journal of molecular sciences · 2021Review
- The protective effect ofPeerJ · 2021Article
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- Harnessing the effects of endurance exercise to optimize cognitive health: Fundamental insights from Dr. Mark P. Mattson.Ageing research reviews · 2020Review
- Oxidative DNA damage is concurrently repaired by base excision repair (BER) and apyrimidinic endonuclease 1 (APE1)-initiated nonhomologous end joining (NHEJ) in cortical neurons.Neuropathology and applied neurobiology · 2020Article
- On the epigenetic role of guanosine oxidation.Redox biology · 2020Review
- Lamin A/C promotes DNA base excision repair.Nucleic acids research · 2019Article
- Calcium dysregulation mediates mitochondrial and neurite outgrowth abnormalities in SOD2 deficient embryonic cerebral cortical neurons.Cell death and differentiation · 2019Article
- Incretin Mimetics as Rational Candidates for the Treatment of Traumatic Brain Injury.ACS pharmacology & translational science · 2019Article
- Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States.Cell metabolism · 2018Review
- The Emerging Role of GLP-1 Receptors in DNA Repair: Implications in Neurological Disorders.International journal of molecular sciences · 2017Review
- Brain metabolism in health, aging, and neurodegeneration.The EMBO journal · 2017Review
- DNA polymerase β decrement triggers death of olfactory bulb cells and impairs olfaction in a mouse model of Alzheimer's disease.Aging cell · 2017Article
- Oxidative stress-induced CREB upregulation promotes DNA damage repair prior to neuronal cell death protection.Molecular and cellular biochemistry · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glutamate, the major excitatory neurotransmitter in the brain, activates receptors coupled to membrane depolarization and Ca(2+) influx that mediates functional responses of neurons including processes such as learning and memory. Here we show that reversible nuclear oxidative DNA damage occurs in cerebral cortical neurons in response to transient glutamate receptor activation using non-toxic physiological levels of glutamate. This DNA damage was prevented by intracellular Ca(2+) chelation, the mitochondrial superoxide dismutase mimetic MnTMPyP (Mn-5,10,15,20-tetra(4-pyridyl)-21H,23H-porphine chloride tetrakis(methochloride)), and blockade of the permeability transition pore. The repair of glutamate-induced DNA damage was associated with increased DNA repair activity and increased mRNA and protein levels of apurinic endonuclease 1 (APE1). APE1 knockdown induced accumulation of oxidative DNA damage after glutamate treatment, suggesting that APE1 is a key repair protein for glutamate-induced DNA damage. A cAMP-response element-binding protein (CREB) binding sequence is present in the Ape1 gene (encodes APE1 protein) promoter and treatment of neurons with a Ca(2+)/calmodulin-dependent kinase inhibitor (KN-93) blocked the ability of glutamate to induce CREB phosphorylation and APE1 expression. Selective depletion of CREB using RNA interference prevented glutamate-induced up-regulation of APE1. Thus, glutamate receptor stimulation triggers Ca(2+)- and mitochondrial reactive oxygen species-mediated DNA damage that is then rapidly repaired by a mechanism involving Ca(2+)-induced, CREB-mediated APE1 expression. Our findings reveal a previously unknown ability of neurons to efficiently repair oxidative DNA lesions after transient activation of glutamate receptors.
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