ArticleLife (Basel, Switzerland)2024
Enrichment of H3S28p and H3K9me2 Epigenetic Marks on Inflammatory-Associated Gene Promoters in Response to Severe Burn Injury.
Article in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
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9 authors.
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Abstract
backgroundSevere burns activate systemic inflammation and lead to an increase in cytokine levels. Epigenetic elements are key regulators of inflammation; however, their involvement in severe burns has not been studied. In this work, we aimed to unveil the histone H3 posttranslational modifications (PTM) profile and their enrichment in promoters of inflammatory genes in response to severe burns.
methodsThe levels of H3 PTMs were analyzed by ELISA assays in circulating cells from burn patients. ChIP assays were conducted to evaluate the enrichment of H3K9me2 and H3S28p at the promoter of CXCL8, IL-17, TNFA, IL-6, FOS, and IL-1B genes.
resultsWe found that eight H3 PTMs decreased at 5 days post-burn. Burn patients showed a decreased enrichment of H3K9me2 in CXCL8, IL-17, and TNFA promoters, whereas IL-6, FOS, and IL-1B promoters displayed an H3S28p enrichment diminution during the first 10 days post-burn. Interestingly, burn-injured septic patients exhibited an increased enrichment of H3K9me2 in TNFA, IL-1B, CXCL8, and IL-17 promoters, whereas H3S28p was increased in promoters of TNFA and IL-1B at 1 dpb.
conclusionSevere burns trigger epigenetic changes and differential H3 PTM enrichment at inflammation gene promoters. Epigenetic misregulation of H3 may be involved in sepsis occurrence after severe burn injury.
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