ArticleThe Journal of biological chemistry2010
Hypoxic repression of endothelial nitric-oxide synthase transcription is coupled with eviction of promoter histones.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 146 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
- Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Endothelial dysfunction in cardiovascular diseases: mechanisms and in vitro models.Molecular and cellular biochemistry · 2025Review
- Metaboloepigenetics: Role in the Regulation of Flow-Mediated Endothelial (Dys)Function and Atherosclerosis.Cells · 2025Review
- The Impact of Modifiable Risk Factors on the Endothelial Cell Methylome and Cardiovascular Disease Development.Frontiers in bioscience (Landmark edition) · 2025Review
- Metabolic alterations of endothelial cells under transient and persistent hypoxia: study using a 3D microvessels-on-chip model.Tissue barriers · 2025Article
- Promotion of nitric oxide production: mechanisms, strategies, and possibilities.Frontiers in physiology · 2025Review
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Hypoxia-induced signaling in the cardiovascular system: pathogenesis and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- The coming of age of liquid biopsy in neuro-oncology.Brain : a journal of neurology · 2023Article
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- 2'-5' oligoadenylate synthetase‑like 1 (OASL1) protects against atherosclerosis by maintaining endothelial nitric oxide synthase mRNA stability.Nature communications · 2022Article
- NOGOB receptor deficiency increases cerebrovascular permeability and hemorrhage via impairing histone acetylation-mediated CCM1/2 expression.The Journal of clinical investigation · 2022Article
- Review
- Endothelial Dysfunction Driven by Hypoxia-The Influence of Oxygen Deficiency on NO Bioavailability.Biomolecules · 2021Review
- Specific arterio-venous transcriptomic and ncRNA-RNA interactions in human umbilical endothelial cells: A meta-analysis.iScience · 2021Article
- The U-shaped association of altitudes with prevalence of hypertension among residents in Tibet, China.Journal of human hypertension · 2021Article
- The link among microbiota, epigenetics, and disease development.Environmental science and pollution research international · 2021Review
- The Role of Histone Protein Acetylation in Regulating Endothelial Function.Frontiers in cell and developmental biology · 2021Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedHo, J J Jr [corrected to Ho, J J David]
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Hypoxia elicits endothelial dysfunction, in part, through reduced expression of endothelial nitric-oxide synthase (eNOS). Here we present evidence that hypoxia causes a rapid decrease in the transcription of the eNOS/NOS3 gene, accompanied by decreased acetylation and lysine 4 (histone H3) methylation of eNOS proximal promoter histones. Surprisingly, we demonstrate that histones are rapidly evicted from the eNOS proximal promoter during hypoxia. We also demonstrate endothelium-specific H2A.Z incorporation at the eNOS promoter and find that H2A.Z is also evicted by hypoxic stimulation. After longer durations of hypoxia, histones are reincorporated at the eNOS promoter, but these histones lack substantial histone acetylation. Additionally, we identify a key role for the chromatin remodeler, BRG1, in re-establishing eNOS expression following reoxygenation of hypoxic cells. We posit that post-translational histone modifications are required to maintain constitutive eNOS transcriptional activity and that histone eviction rapidly resets histone marks and is a proximal event in the hypoxic repression of eNOS. Although nucleosome eviction has been reported in models of transcriptional activation, the observation that eviction can also accompany transcriptional repression in hypoxic mammalian cells argues that eviction may be broadly relevant to both positive and negative changes in transcription.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.