ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Histone deacetylase 1 reduces NO production in endothelial cells via lysine deacetylation of NO synthase 3.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Histone H4K5 deacetylation by enhanced HDAC1 expression drives endothelial inflammation in diabetes through repression of the KLF2-eNOS axis.Human cell · 2026Article
- Mechanisms of Okanin against wound healing based on network pharmacology, molecular docking and molecular dynamics simulation.Scientific reports · 2025Article
- Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.Cells · 2025Review
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Endothelial histone deacetylase 1 activity impairs kidney microvascular NO signaling in rats fed a high-salt diet.Acta physiologica (Oxford, England) · 2024Article
- Analysis of global DNA methylation and epigenetic modifiers (DNMTs and HDACs) in human foetal endothelium exposed to gestational and type 2 diabetes.Epigenetics · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- HDAC1: an environmental sensor regulating endothelial function.Cardiovascular research · 2022Review
- Nitric-Oxide-Mediated Signaling in Podocyte Pathophysiology.Biomolecules · 2022Review
- HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis.Scientific reports · 2021Article
- Altered endothelial dysfunction-related miRs in plasma from ME/CFS patients.Scientific reports · 2021Article
- HDAC1-mediated deacetylation of HIF1α prevents atherosclerosis progression by promoting miR-224-3p-mediated inhibition of FOSL2.Molecular therapy. Nucleic acids · 2021Article
- High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021Article
- Oxidative Stress and New Pathogenetic Mechanisms in Endothelial Dysfunction: Potential Diagnostic Biomarkers and Therapeutic Targets.Journal of clinical medicine · 2020Review
- Early Programming of Adult Systemic Essential Hypertension.International journal of molecular sciences · 2020Review
- Up-regulation of HDACs, a harbinger of uraemic endothelial dysfunction, is prevented by defibrotide.Journal of cellular and molecular medicine · 2020Article
- Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review.Frontiers in cell and developmental biology · 2020Review
- Role of Nitric Oxide and Hydrogen Sulfide in Ischemic Stroke and the Emergent Epigenetic Underpinnings.Molecular neurobiology · 2019Review
- Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2019Review
- Dynamic regulation of lysine acetylation: the balance between acetyltransferase and deacetylase activities.American journal of physiology. Renal physiology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The lysine acetylation state of nonhistone proteins may be regulated through histone deacetylases (HDACs). Evidence suggests that nitric oxide (NO) synthase 3 (NOS3; endothelial NOS) is posttranslationally lysine acetylated, leading to increased NO production in the endothelium. We tested the hypothesis that NOS3 is lysine acetylated and that upregulated HDAC1-mediated deacetylation leads to reduced NO production in endothelial cells. We determined that NOS3 is basally lysine acetylated in cultured bovine aortic endothelial cells (BAECs). In BAECs, HDAC1 is expressed in the nucleus and cytosol and forms a novel protein-protein interaction with NOS3. Overexpression of HDAC1 in BAECs resulted in a significant reduction in NOS3 lysine acetylation (control = 1.0 ± 0.1 and HDAC1 = 0.59 ± 0.08 arbitrary units, P < 0.01) and significantly blunted basal nitrite production (control 287.7 ± 29.1 and HDAC1 172.4 ± 31.7 pmol·mg(-1)·h(-1), P < 0.05) as well as attenuating endothelin-1-stimulated nitrite production (control = 481.8 ± 50.3 and HDAC1 243.1 ± 48.2 pmol·mg(-1)·h(-1), P < 0.05). While HDAC1 knockdown with small-interfering RNA resulted in no change in NOS3 acetylation level, yet increased basal nitrite production (730.6 ± 99.1 pmol·mg(-1)·h(-1)) and further exaggerated increases in endothelin-1 stimulated nitrite production (1276.9 ± 288.2 pmol·mg(-1)·h(-1)) was observed. Moreover, overexpression or knockdown of HDAC1 resulted in no significant effect on NOS3 protein expression or NOS3 phosphorylation sites T497, S635, or S1179. Thus these data indicate that upregulated HDAC1 decreases NOS3 activity, most likely through direct lysine deacetylation of NOS3. We propose that HDAC1-mediated deacetylation of NOS3 may represent a novel target for endothelial dysfunction.
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