ArticlePhysiological genomics2018
Persistent pulmonary hypertension alters the epigenetic characteristics of endothelial nitric oxide synthase gene in pulmonary artery endothelial cells in a fetal lamb model.
Article in Physiological genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanical forces orchestrate the epigenetic landscape of oral mesenchymal stem/progenitor cell fate in dental and periodontal tissues.Frontiers in cell and developmental biology · 2026Review
- Isoflavones Effects on Vascular and Endothelial Outcomes: How Is the Gut Microbiota Involved?Pharmaceuticals (Basel, Switzerland) · 2024Review
- Switch-Independent 3A: An Epigenetic Regulator in Cancer with New Implications for Pulmonary Arterial Hypertension.Biomedicines · 2023Review
- Unraveling the epigenetic landscape of pulmonary arterial hypertension: implications for personalized medicine development.Journal of translational medicine · 2023Review
- Integrating epigenetics and metabolomics to advance treatments for pulmonary arterial hypertension.Biochemical pharmacology · 2022Review
- Differences in the expression of DNA methyltransferases and demethylases in leukocytes and the severity of pulmonary arterial hypertension between ethnic groups.Physiological reports · 2022Article
- Association of asymmetric dimethylarginine with the pathological process of persistent pulmonary hypertension of the newborn.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Article
- Mechanical Cues Regulate Histone Modifications and Cell Behavior.Stem cells international · 2022Review
- Epigenetic Regulation of Endothelial Dysfunction and Inflammation in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2021Review
- Decreased Cyclic Guanosine Monophosphate-Protein Kinase G Signaling Impairs Angiogenesis in a Lamb Model of Persistent Pulmonary Hypertension of the Newborn.American journal of respiratory cell and molecular biology · 2021Article
- Nitric Oxide-cGMP Pathway Modulation in an Experimental Model of Hypoxic Pulmonary Hypertension.Journal of cardiovascular pharmacology and therapeutics · 2021Article
- The Role of Histone Protein Acetylation in Regulating Endothelial Function.Frontiers in cell and developmental biology · 2021Review
- DNA methyltransferase 3B deficiency unveils a new pathological mechanism of pulmonary hypertension.Science advances · 2020Article
- Mechanical regulation of histone modifications and cell plasticity.Current opinion in solid state & materials science · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Decreased expression of endothelial nitric oxide synthase (eNOS), a key mediator of perinatal transition, characterizes persistent pulmonary hypertension of the newborn (PPHN) in neonates and a fetal lamb model; the mechanisms are unclear. We investigated whether increased DNA CpG methylation at the eNOS promoter in estrogen response elements (EREs) and altered histone code together contribute to decreased eNOS expression in PPHN. We isolated pulmonary artery endothelial cells (PAEC) from fetal lambs with PPHN induced by prenatal ductus arteriosus constriction from 128 to 136 days gestation or gestation-matched twin controls. We measured right ventricular systolic pressure (RVSP) and Fulton index and determined eNOS expression in PAEC in control and PPHN lambs. We determined DNA CpG methylation by pyrosequencing and activity of ten eleven translocase demethylases (TET) by colorimetric assay. We quantified the occupancy of transcription factors, specificity protein 1 (Sp1), and estrogen receptors and density of four histone marks around Sp1 binding sites by chromatin immunoprecipitation (ChIP) assays. Fetal lambs with PPHN developed increased RVSP and Fulton index. Levels of eNOS mRNA and protein were decreased in PAEC from PPHN lambs. PPHN significantly increased the DNA CpG methylation in eNOS promoter and decreased TET activity in PAEC. PPHN decreased Sp1 occupancy and density of the active mark, lysine 12 acetylation of histone 4, and increased density of the repression mark, lysine 9 trimethylation of histone 3 around Sp1 binding sites in eNOS promoter. These results suggest that epigenetic modifications are primed to decrease Sp1 binding at the eNOS gene promoter in PPHN.
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