ArticleCardiovascular research2011
Foetal nicotine exposure causes PKCε gene repression by promoter methylation in rat hearts.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Efficacy and safety of ephedra-containing oral medications: a systematic review, meta-analysis, and exploratory dose-response analysis for weight reduction.Frontiers in pharmacology · 2024Pooled it
- Nicotine Exposure During Gestation: From Placental Dysfunction to Long-Term Neurobehavioral Outcomes.Birth defects research · 2026Review
- DNA Methylation and Fetal Programming of Cardiovascular Disease: From Congenital Heart Diseases to Adult Cardiovascular Dysfunction.Reviews in cardiovascular medicine · 2026Review
- State-Dependent DNA Methylation Signatures Distinguish Acute from Stable Coronary Syndromes.International journal of molecular sciences · 2026Article
- Early growth response-1: Key mediators of cell death and novel targets for cardiovascular disease therapy.Frontiers in cardiovascular medicine · 2023Review
- Single molecule characterization of the binding kinetics of a transcription factor and its modulation by DNA sequence and methylation.Nucleic acids research · 2021Article
- Adverse effects of fetal exposure of electronic-cigarettes and high-fat diet on male neonatal hearts.Experimental and molecular pathology · 2021Article
- Improving translational research in sex-specific effects of comorbidities and risk factors in ischaemic heart disease and cardioprotection: position paper and recommendations of the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2021Review
- Does Prenatal Exposure to CNS Stimulants Increase the Risk of Cardiovascular Disease in Adult Offspring?Frontiers in cardiovascular medicine · 2021Review
- Mechanism underlying increased cardiac extracellular matrix deposition in perinatal nicotine-exposed offspring.American journal of physiology. Heart and circulatory physiology · 2020Article
- Inhibition of Autophagy Signaling via 3-methyladenine Rescued Nicotine-Mediated Cardiac Pathological Effects and Heart Dysfunctions.International journal of biological sciences · 2020Article
- Long-term exposure to high altitude hypoxia during pregnancy increases fetal heart susceptibility to ischemia/reperfusion injury and cardiac dysfunction.International journal of cardiology · 2019Article
- Gestational Hypoxia and Developmental Plasticity.Physiological reviews · 2018Review
- Role of DNA methylation in perinatal nicotine-induced development of heart ischemia-sensitive phenotype in rat offspring.Oncotarget · 2017Article
- Nicotine facilitates VSMC dysfunction through a miR-200b/RhoGDIA/cytoskeleton module.Scientific reports · 2017Article
- Inhibition of Gata4 and Tbx5 by Nicotine-Mediated DNA Methylation in Myocardial Differentiation.Stem cell reports · 2017Article
- Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart.PloS one · 2017Article
- In utero exposure to maternal smoking is associated with DNA methylation alterations and reduced neuronal content in the developing fetal brain.Epigenetics & chromatin · 2017Article
- Antenatal hypoxia induces epigenetic repression of glucocorticoid receptor and promotes ischemic-sensitive phenotype in the developing heart.Journal of molecular and cellular cardiology · 2016Article
- Protective Effect of Antenatal Antioxidant on Nicotine-Induced Heart Ischemia-Sensitive Phenotype in Rat Offspring.PloS one · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsfoetal nicotine exposure results in decreased protein kinase C epsilon (PKCε) expression and increased cardiac vulnerability to ischaemia and reperfusion injury in adult rat offspring. The present study tested the hypothesis that maternal nicotine administration causes increased promoter methylation of the PKCε gene resulting in PKCε repression in the heart. METHODS AND
resultsnicotine treatment of pregnant rats starting at day 4 of gestation increased the methylation of the Egr-1 binding site at the PKCε gene promoter and decreased PKCε protein and mRNA abundance in near-term foetal hearts. Methylation of the Egr-1 binding site reduced Egr-1 binding to the PKCε promoter in the heart. Site-specific deletion of the Egr-1 binding site significantly decreased PKCε promoter activity. The effects of nicotine were sustained in the heart of adult offspring. Ex vivo studies found no direct effect of nicotine on PKCε gene expression. However, maternal nicotine administration increased norepinephrine content in the foetal heart. Treatment of isolated foetal hearts with norepinephrine resulted in the same effects of increased methylation of the Egr-1 binding site and PKCε gene repression in the heart. 5-Aza-2'-deoxycytidine inhibited the norepinephrine-induced increase in methylation of the Egr-1 binding site and restored Egr-1 binding and PKCε gene expression to the control levels.
conclusionthis study demonstrates that prolonged nicotine exposure increases the sympathetic neurotransmitter release in the foetal heart and causes programming of PKCε gene repression through promoter methylation, linking maternal smoking to pathophysiological consequences in the offspring heart.
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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.