ArticleThe Journal of biological chemistry2005
Role of histone deacetylation in cell-specific expression of endothelial nitric-oxide synthase.
Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 93 citations in OpenAlex.
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- Recent advancements and comprehensive analyses of butyric acid in cardiovascular diseases.Frontiers in cardiovascular medicine · 2025Review
- Epigenetic DNA Methylation and Protein Homocysteinylation: Key Players in Hypertensive Renovascular Damage.International journal of molecular sciences · 2024Review
- Rescuing lung development through embryonic inhibition of histone acetylation.Science translational medicine · 2024Article
- Epigenetic Signatures in Arterial Hypertension: Focus on the Microvasculature.International journal of molecular sciences · 2023Review
- HDAC1: an environmental sensor regulating endothelial function.Cardiovascular research · 2022Review
- Epigenetic Alterations in Pediatric Sleep Apnea.International journal of molecular sciences · 2021Review
- Gut microbial-derived short-chain fatty acids and bone: a potential role in fracture healing.European cells & materials · 2021Review
- ΔNp63α promotes the expression and nuclear translocation of PTEN, leading to cisplatin resistance in oral cancer cells.American journal of translational research · 2020Article
- Role of Nitric Oxide and Hydrogen Sulfide in Ischemic Stroke and the Emergent Epigenetic Underpinnings.Molecular neurobiology · 2019Review
- New Therapeutic Implications of Endothelial Nitric Oxide Synthase (eNOS) Function/Dysfunction in Cardiovascular Disease.International journal of molecular sciences · 2019Review
- Epigenetic Mechanisms and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Review
- Knockdown of Yin Yang 1 enhances anticancer effects of cisplatin through protein phosphatase 2A-mediated T308 dephosphorylation of AKT.Cell death & disease · 2018Article
- Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function.Nature communications · 2018Article
- Cavin-1 regulates caveolae-mediated LDL transcytosis: crosstalk in an AMPK/eNOS/ NF-κB/Sp1 loop.Oncotarget · 2017Article
- Histone deacetylase inhibitors promote eNOS expression in vascular smooth muscle cells and suppress hypoxia-induced cell growth.Journal of cellular and molecular medicine · 2017Article
- The role of epigenetics in the endothelial cell shear stress response and atherosclerosis.The international journal of biochemistry & cell biology · 2015Review
- Mechanisms of Histone Deacetylase Inhibitor-Regulated Gene Expression in Cancer Cells.Antioxidants & redox signaling · 2015Review
- Histone deacetylase 1 reduces NO production in endothelial cells via lysine deacetylation of NO synthase 3.American journal of physiology. Heart and circulatory physiology · 2014Article
- Endothelial heterogeneity in the umbilico-placental unit: DNA methylation as an innuendo of epigenetic diversity.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Histone acetylation plays an important role in chromatin remodeling and gene expression. The molecular mechanisms involved in cell-specific expression of endothelial nitric-oxide synthase (eNOS) are not fully understood. In this study we investigated whether histone deacetylation was involved in repression of eNOS expression in non-endothelial cells. Induction of eNOS expression by histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in all four different types of non-endothelial cells examined. Chromatin immunoprecipitation assays showed that the induction of eNOS expression by TSA was accompanied by a remarkable increase of acetylation of histone H3 associated with the eNOS 5'-flanking region in the non-endothelial cells. Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2'-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells. The proximal Sp1 site is critical for basal activity of eNOS promoter. The induction of eNOS by inhibition of HDACs in non-endothelial cells, however, appeared not mediated by the changes in Sp1 DNA binding activity. We further showed that Sp1 bound to the endogenous eNOS promoter and associated with HDAC1 in non-endothelial HeLa cells. Combined TSA and AzadC treatment increased Sp1 binding to the endogenous eNOS promoter but decreased the association between HDAC1 and Sp1 in HeLa cells. Our data suggest that HDAC1 plays a critical role in eNOS repression, and the proximal Sp1 site may serve a key target for HDCA1-mediated eNOS repression in non-endothelial cells.
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