ArticleThe American journal of pathology2014
Combinatorial therapy with acetylation and methylation modifiers attenuates lung vascular hyperpermeability in endotoxemia-induced mouse inflammatory lung injury.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Immune responses to azacytidine in animal models of inflammatory disorders: a systematic review.Journal of translational medicine · 2021Pooled it
- Implications of Protein Posttranslational Modifications in Sepsis-Induced Acute Lung Injury and Acute Respiratory Distress Syndrome.Shock (Augusta, Ga.) · 2025Review
- Molecular mechanisms and functions of protein acetylation in sepsis and sepsis-associated organ dysfunction.Cellular & molecular biology letters · 2025Review
- 5-Aza-2'-Deoxycytidine Ameliorates Choroidal Neovascularization by Inhibiting the Wnt/β-Catenin Signaling Pathway.Investigative ophthalmology & visual science · 2024Article
- Zinc-Dependent Histone Deacetylases in Lung Endothelial Pathobiology.Biomolecules · 2024Review
- Post-translational modifications in sepsis-induced organ dysfunction: mechanisms and implications.Frontiers in immunology · 2024Review
- Endothelial FoxM1 reactivates aging-impaired endothelial regeneration for vascular repair and resolution of inflammatory lung injury.Science translational medicine · 2023Article
- Inhibition of DNA methylation attenuates lung ischemia-reperfusion injury after lung transplantation.The Journal of international medical research · 2023Article
- Aquaporin-5 Dynamic Regulation.International journal of molecular sciences · 2023Review
- Targeting epigenetic regulators for inflammation: Mechanisms and intervention therapy.MedComm · 2022Review
- AQP5-1364A/C Polymorphism AffectsInternational journal of molecular sciences · 2022Article
- NOGOB receptor deficiency increases cerebrovascular permeability and hemorrhage via impairing histone acetylation-mediated CCM1/2 expression.The Journal of clinical investigation · 2022Article
- Inhibitors of DNA Methylation.Advances in experimental medicine and biology · 2022Review
- Role of Caveolin-1 in Sepsis - A Mini-Review.Frontiers in immunology · 2022Review
- Role of HDAC6 inhibition in sepsis-induced acute respiratory distress syndrome (Review).Experimental and therapeutic medicine · 2021Review
- Infectious Keratitis: An Update on Role of Epigenetics.Frontiers in immunology · 2021Review
- The Role of Histone Protein Acetylation in Regulating Endothelial Function.Frontiers in cell and developmental biology · 2021Review
- Molecular Mechanisms of Vascular Damage During Lung Injury.Advances in experimental medicine and biology · 2021Review
- The Role of Host Cell DNA Methylation in the Immune Response to Bacterial Infection.Frontiers in immunology · 2021Review
- The Surviving Sepsis Campaign: Basic/Translational Science Research Priorities.Critical care medicine · 2020Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Impairment of tissue fluid homeostasis and migration of inflammatory cells across the vascular endothelial barrier are crucial factors in the pathogenesis of acute lung injury (ALI). The goal for treatment of ALI is to target pathways that lead to profound dysregulation of the lung endothelial barrier. Although studies have shown that chemical epigenetic modifiers can limit lung inflammation in experimental ALI models, studies to date have not examined efficacy of a combination of DNA methyl transferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor trichostatin A (herein referred to as Aza+TSA) after endotoxemia-induced mouse lung injury. We tested the hypothesis that treatment with Aza+TSA after lipopolysaccharide induction of ALI through epigenetic modification of lung endothelial cells prevents inflammatory lung injury. Combinatorial treatment with Aza+TSA mitigated the increased endothelial permeability response after lipopolysaccharide challenge. In addition, we observed reduced lung inflammation and lung injury. Aza+TSA also significantly reduced mortality in the ALI model. The protection was ascribed to inhibition of the eNOS-Cav1-MLC2 signaling pathway and enhanced acetylation of histone markers on the vascular endothelial-cadherin promoter. In summary, these data show for the first time the efficacy of combinatorial Aza+TSA therapy in preventing ALI in lipopolysaccharide-induced endotoxemia and raise the possibility of an essential role of DNA methyl transferase and histone deacetylase in the mechanism of ALI.
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Registered trials
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