ArticleJournal of translational medicine2014
Hypermethylation of DDAH2 promoter contributes to the dysfunction of endothelial progenitor cells in coronary artery disease patients.
Article in Journal of translational medicine, 2014. 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, 30 citations in OpenAlex.
- Unraveling Atherosclerosis through Multi-omics: Systematic Insights into the Unique Applications and Clinical Perspectives.Current atherosclerosis reports · 2026Review
- Genetic link between metabolic syndrome and coronary artery disease: Insights from genome-wide cross-trait analysis.Global medical genetics · 2026Article
- Exercise-mediated epigenetic modifications in cardiovascular diseases.Epigenomics · 2025Review
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- Genetics of PlGF plasma levels highlights a role of its receptors and supports the link between angiogenesis and immunity.Scientific reports · 2021Article
- Roles and Mechanisms of DNA Methylation in Vascular Aging and Related Diseases.Frontiers in cell and developmental biology · 2021Review
- Methylation of CpG sites in C1QTNF1 (C1q and tumor necrosis factor related protein 1) differs by gender in acute coronary syndrome in Han population: a case-control study.Genes & genomics · 2020Article
- Hyperhomocysteinemia induced endothelial progenitor cells dysfunction through hyper-methylation of CBS promoter.Biochemical and biophysical research communications · 2019Article
- Machine learning algorithm-based risk prediction model of coronary artery disease.Molecular biology reports · 2018Article
- Activation of ATP-sensitive potassium channels facilitates the function of human endothelial colony-forming cells via CaJournal of cellular and molecular medicine · 2017Article
- Oxidative stress and epigenetic modifications in the pathogenesis of diabetic retinopathy.Progress in retinal and eye research · 2015Review
- Epigenetic reprogramming in atherosclerosis.Current atherosclerosis reports · 2015Review
- Demethylation treatment restores erectile function in a rat model of hyperhomocysteinemia.Asian journal of andrologyArticle
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCirculating endothelial progenitor cells (EPCs) may be a biomarker for vascular function and cardiovascular risk in patients with coronary artery disease (CAD). Dimethylarginine dimethylaminohydrolase 2 (DDAH2) regulates the function of EPCs. This study aimed to examine whether hypermethylation of DDAH2 promoter contributes to impaired function of EPCs in CAD patients.
methodsPeripheral blood mono-nuclear cells from 25 CAD patients and 15 healthy volunteers were collected and differentiated into EPCs. EPCs were tested for their adhesive capability. DDAH2 mRNA expression was analyzed by real-time PCR, and the methylation of DDAH2 promoter was detected by bisulfite genomic sequencing.
resultsDDAH2 promoter in EPCs from CAD patients was hypermethylated and the methylation level was negatively correlated to DDAH2 mRNA level and adhesion function of EPCs. Homocysteine impaired the adhesion function of EPCs, accompanied by lower DDAH2 expression and higher methylation level of DDAH2 promoter, compared to controls. These effects of homocysteine were reversed by pretreatment with Aza, an inhibitor of DNA methyltransferase.
conclusionHypermethylation in DDAH2 promoter is positively correlated to the dysfunction of EPCs in CAD patients. Homocysteine disrupts EPCs function via inducing the hypermethylation of DDAH2 promoter, suggesting a key role of epigenetic mechanism in the progression of atherosclerosis.
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