ArticleLupus science & medicine2016
Histone H2AX phosphorylation as a measure of DNA double-strand breaks and a marker of environmental stress and disease activity in lupus.
Article in Lupus science & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Fatigue outcomes with anifrolumab in low-disease-activity SLE: DNA damage in plasmacytoid dendritic cells as a candidate biomarker for responders.Lupus science & medicine · 2026Article
- Sublethal DNA damage switches off B cell effector programs in an RA-FLS-PBMC co-culture.Cell death discovery · 2026Article
- Review
- Genotoxic stressors mimicking synovial microenvironment modulate B cell fate in RA-FLS co-culture.Frontiers in immunology · 2026Article
- Asymptomatic herpes simplex virus brain infection elicits cellular senescence phenotypes in the central nervous system of mice suffering multiple sclerosis-like disease.Communications biology · 2024Article
- Enhanced GATA4 expression in senescent systemic lupus erythematosus monocytes promotes high levels of IFNα production.Frontiers in immunology · 2024Article
- Molecular pathways identified from single nucleotide polymorphisms demonstrate mechanistic differences in systemic lupus erythematosus patients of Asian and European ancestry.Scientific reports · 2023Article
- ATR-mediated DNA damage responses underlie aberrant B cell activity in systemic lupus erythematosus.Science advances · 2022Article
- The Role of Oxidative Stress in Epigenetic Changes Underlying Autoimmunity.Antioxidants & redox signaling · 2022Review
- DNA Damage Response in the Adaptive Arm of the Immune System: Implications for Autoimmunity.International journal of molecular sciences · 2021Review
- Focus on the Gut-Kidney Axis in Health and Disease.Frontiers in medicine · 2020Review
- Increased Expression of EZH2 Is Mediated by Higher Glycolysis and mTORC1 Activation in Lupus CD4Immunometabolism · 2020Article
- Metabolic abnormalities and oxidative stress in lupus.Current opinion in rheumatology · 2017Review
- Defective DNA repair and chromatin organization in patients with quiescent systemic lupus erythematosus.Arthritis research & therapy · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDefective or inefficient DNA double-strand break (DSB) repair results in failure to preserve genomic integrity leading to apoptotic cell death, a hallmark of systemic lupus erythematosus (SLE). Compelling evidence linked environmental factors that increase oxidative stress with SLE risk and the formation of DSBs. In this study, we sought to further explore genotoxic stress sensitivity in SLE by investigating DSB accumulation as a marker linking the effect of environmental stressors and the chromatin microenvironment.
methodsDSBs were quantified in peripheral blood mononuclear cell subsets from patients with SLE, healthy controls, and patients with rheumatoid arthritis (RA) by measuring phosphorylated H2AX (phospho-H2AX) levels with flow cytometry. Phospho-H2AX levels were assessed in G0/G1, S and G2 cell-cycle phases using propidium iodide staining, and after oxidative stress using 0.5 µM hydrogen peroxide exposure for 0, 2, 5, 10, 30 and 60 min.
resultsDSB levels were significantly increased in CD4+ T cells, CD8+ T cells and monocytes in SLE compared with healthy controls (p=2.16×10(-4), 1.68×10(-3) and 4.74×10(-3), respectively) and RA (p=1.05×10(-3), 1.78×10(-3) and 2.43×10(-2), respectively). This increase in DSBs in SLE was independent of the cell-cycle phase, and correlated with disease activity. In CD4+ T cells, CD8+ T cells and monocytes, oxidative stress exposure induced significantly higher DSB accumulation in SLE compared with healthy controls (60 min; p=1.64×10(-6), 8.11×10(-7) and 2.04×10(-3), respectively).
conclusionsOur data indicate that SLE T cells and monocytes have increased baseline DSB levels and an increased sensitivity to acquiring DSBs in response to oxidative stress. Although the mechanism underlying DSB sensitivity in SLE requires further investigation, accumulation of DSB may serve a biomarker for disease activity in SLE and help explain increased apoptotic cell accumulation in this disease.
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