ArticleJournal of cellular and molecular medicine2016
Trichostatin A, a histone deacetylase inhibitor suppresses NADPH Oxidase 4-Derived Redox Signalling and Angiogenesis.
Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Identification and Validation of Candidate Biomarkers Co-expressed with Creatine Metabolism-Related Genes in Ischemic Stroke Based on Transcriptomics Data.Molecular neurobiology · 2026Article
- Diabetic retinopathy: shaped by the "hidden hand" of post-translational modifications.Molecular neurodegeneration · 2026Review
- Exploration of key stress granule-related genes in chronic sinusitis based on transcriptomics.Scientific reports · 2026Article
- Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Trichostatin A suppresses hearing loss by reducing oxidative stress and inflammation in an Alport syndrome model.PloS one · 2025Article
- The role of NADPH oxidase 1 in alcohol-induced oxidative stress injury of intestinal epithelial cells.Cell biology and toxicology · 2023Article
- PGC-1α inhibits M2 macrophage polarization and alleviates liver fibrosis following hepatic ischemia reperfusion injury.Cell death discovery · 2023Article
- Nox4 as a novel therapeutic target for diabetic vascular complications.Redox biology · 2023Review
- Review
- Bicalutamide Exhibits Potential to Damage Kidney via Destroying Complex I and Affecting Mitochondrial Dynamics.Journal of clinical medicine · 2021Article
- Sulforaphane Ameliorates Diabetes-Induced Renal Fibrosis through Epigenetic Up-Regulation of BMP-7.Diabetes & metabolism journal · 2021Article
- Activated Histone Acetyltransferase p300/CBP-Related Signalling Pathways Mediate Up-Regulation of NADPH Oxidase, Inflammation, and Fibrosis in Diabetic Kidney.Antioxidants (Basel, Switzerland) · 2021Article
- The Role of Histone Protein Acetylation in Regulating Endothelial Function.Frontiers in cell and developmental biology · 2021Review
- Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review.Frontiers in cell and developmental biology · 2020Review
- Impact of HDAC Inhibitors on Protein Quality Control Systems: Consequences for Precision Medicine in Malignant Disease.Frontiers in cell and developmental biology · 2020Review
- Article
- Age-related macular degeneration (AMD) mitochondria modulate epigenetic mechanisms in retinal pigment epithelial cells.Experimental eye research · 2019Article
- From molecular promise to preclinical results: HDAC inhibitors in the race for healthy aging drugs.EMBO molecular medicine · 2019Review
- Histone Acetyltransferase-Dependent Pathways Mediate Upregulation of NADPH Oxidase 5 in Human Macrophages under Inflammatory Conditions: A Potential Mechanism of Reactive Oxygen Species Overproduction in Atherosclerosis.Oxidative medicine and cellular longevity · 2019Article
- Epigenetic regulation of vascular NADPH oxidase expression and reactive oxygen species production by histone deacetylase-dependent mechanisms in experimental diabetes.Redox biology · 2018Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) inhibitors are known to suppress abnormal development of blood vessels. Angiogenic activity in endothelial cells depends upon NADPH oxidase 4 (Nox4)-dependent redox signalling. We set out to study whether the HDAC inhibitor trichostatin A (TSA) affects Nox4 expression and angiogenesis. Nox4 expression was measured by real time PCR and Western blot analysis in endothelial cells. Hydrogen peroxide (H2 O2 ) was measured by amplex(®) red assay in endothelial cells. Nox4 was knocked down by Nox4 shRNA. In vitro angiogenic activities such migration and tubulogenesis were assessed using wound healing and Matrigel assays, respectively. In vivo angiogenic activity was assessed using subcutaneous sponge assay in C57Bl/6 and Nox4-deficient mice. Trichostatin A reduced Nox4 expression in a time- and concentration-dependent manner. Both TSA and Nox4 silencing decreased Nox4 protein and H2 O2 . Mechanistically, TSA reduced expression of Nox4 via ubiquitination of p300- histone acetyltransferase (p300-HAT). Thus, blocking of the ubiquitination pathway using an inhibitor of ubiquitin-activating enzyme E1 (PYR-41) prevented TSA inhibition of Nox4 expression. Trichostatin A also reduced migration and tube formation, and these effects were not observed in Nox4-deficient endothelial cells. Finally, transforming growth factor beta1 (TGFβ1) enhanced angiogenesis in sponge model in C57BL/6 mice. This response to TGFβ1 was substantially reduced in Nox4-deficient mice. Similarly intraperitoneal infusion of TSA (1 mg/kg) also suppressed TGFβ1-induced angiogenesis in C57BL/6 mice. Trichostatin A reduces Nox4 expression and angiogenesis via inhibition of the p300-HAT-dependent pathway. This mechanism might be exploited to prevent aberrant angiogenesis in diabetic retinopathy, complicated vascular tumours and malformations.
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