Ethanol and Its Metabolites Induce Histone Lysine 9 Acetylation and an Alteration of the Expression of Heart Development-Related Genes in Cardiac Progenitor Cells

Alcohol exposure during pregnancy may cause congenital heart disease (CHD), but the underlying mechanisms are not clear. Recent evidence suggests that ethanol and its metabolites can selectively increase histone H3 acetylation at lysine 9 (H3AcK9) residue in rat hepatocytes. This may be a mechanism...

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Veröffentlicht in:	Cardiovascular toxicology 2010-12, Vol.10 (4), p.268-274
Hauptverfasser:	Zhong, Lilin, Zhu, Jing, Lv, Tiewei, Chen, Guozhen, Sun, Huichao, Yang, Xuefang, Huang, Xupei, Tian, Jie
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetaldehyde Acetaldehyde - toxicity Acetates Acetates - toxicity Acetylation Alcohol Alcohol, Denatured Animals Biomedical and Life Sciences Biomedicine Blotting, Western Cardiology Cell Line Cell Survival - drug effects Chromatin Assembly and Disassembly - drug effects Congenital heart disease Developmental biology DNA methylation Dose-Response Relationship, Drug Effect of alcohol on Epigenetics Ethanol Ethanol - metabolism Ethanol - toxicity Fetal alcohol syndrome Fetus GATA4 Transcription Factor - genetics Gene expression Gene Expression Regulation, Developmental - drug effects Genes Genetic disorders Heart Heart diseases Histones - metabolism Humans Lysine MADS Domain Proteins - genetics Medical research Metabolites Mitochondria, Heart - drug effects Mitochondria, Heart - metabolism Morphology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myogenic Regulatory Factors - genetics Pharmacology/Toxicology Reverse Transcriptase Polymerase Chain Reaction RNA Stem Cells - drug effects Stem Cells - metabolism T-Box Domain Proteins - genetics
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