ArticleNeuropathology and applied neurobiology2020
Oxidative DNA damage is concurrently repaired by base excision repair (BER) and apyrimidinic endonuclease 1 (APE1)-initiated nonhomologous end joining (NHEJ) in cortical neurons.
Article in Neuropathology and applied neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- PAICS mediates DNA damage and cerebellar neuronal loss in C9orf72 amyotrophic lateral sclerosis.Brain : a journal of neurology · 2026Article
- A kinetically inert platinum antitumor agent overcomes mutant p53-driven chemoresistance via oxidative stress-mediated DNA damage.Medical oncology (Northwood, London, England) · 2026Article
- Functional Profiling of DNA Repair Pathways in Lung Cancer Patients Uncovers Radiotherapy-Induced and Cancer-Associated Alterations in Oxidative Lesion Repair.medRxiv : the preprint server for health sciences · 2026Article
- Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.Frontiers in immunology · 2026Review
- Sex-Specific Association Between XPC rs2228001 Polymorphism and Parkinson's Disease Risk in a Mexican Population: A Case-Control Study Exploring Gene-Environment Interactions.Brain sciences · 2025Article
- The silent saboteur: oxidative stress and the path to cognitive dysfunction.Neurodegenerative disease management · 2025Review
- Biological Amyloids Chemically Damage DNA.ACS chemical neuroscience · 2025Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- AUF1 Recognizes 8-Oxo-Guanosine Embedded in DNA and Stimulates APE1 Endoribonuclease Activity.Antioxidants & redox signaling · 2023Article
- Article
- circCIMT Silencing Promotes Cadmium-Induced Malignant Transformation of Lung Epithelial Cells Through the DNA Base Excision Repair Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Article
- DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.International journal of molecular sciences · 2022Review
- Molecular markers of DNA repair and brain metabolism correlate with cognition in centenarians.GeroScience · 2022Article
- Prognostic Assessment of Oxidative Stress-Related Genes in Colorectal Cancer and New Insights into Tumor Immunity.Oxidative medicine and cellular longevity · 2022Article
- APE1/Ref-1 Role in Inflammation and Immune Response.Frontiers in immunology · 2022Review
- 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
- Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsAccumulating studies have suggested that base excision repair (BER) is the major repair pathway of oxidative DNA damage in neurons, and neurons are deficient in other DNA repair pathways, including nucleotide excision repair and homologous recombination repair. However, some studies have demonstrated that neurons could efficiently repair glutamate- and menadione-induced double-strand breaks (DSBs), suggesting that the DSB repair mechanisms might be implicated in neuronal health. In this study, we hypothesized that BER and nonhomologous end joining (NHEJ) work together to repair oxidative DNA damage in neurons.
methodsImmunohistochemistry and confocal microscopy were employed to examine the colocalization of apyrimidinic endonuclease 1 (APE1), histone variant 2AX (γH2AX) and phosphorylated p53-binding protein (53BP1). APE1 inhibitor and shRNA were respectively applied to suppress APE1 activity and protein expression to determine the correlation of APE1 and DSB formation. The neutral comet assay was used to determine and quantitate the formation of DSB.
resultsBoth γH2AX and 53BP1 were upregulated and colocalized with APE1 in the nuclei of rat cortical neurons subjected to menadione-induced oxidative insults. Phospho53BP1 foci were efficiently abolished, but γH2AX foci persisted following the suppression of APE1 activity. Comet assays demonstrated that the inhibition of APE1 decreased the DSB formation.
conclusionsOur results indicate that APE1 can engage the NHEJ mechanism in the repair of oxidative DNA damage in neurons. These findings provide insights into the mechanisms underlying the efficient repair of oxidative DNA damage in neurons despite the high oxidative burden.
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