ArticlePloS one2014
Inhibition of histone H3K9 acetylation by anacardic acid can correct the over-expression of Gata4 in the hearts of fetal mice exposed to alcohol during pregnancy.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Rescuing lung development through embryonic inhibition of histone acetylation.Science translational medicine · 2024Article
- Pyrazole-Curcumin Suppresses Cardiomyocyte Hypertrophy by Disrupting the CDK9/CyclinT1 Complex.Pharmaceutics · 2022Article
- Review
- Interactions between the ERK1/2 signaling pathway and PCAF play a key role in PE‑induced cardiomyocyte hypertrophy.Molecular medicine reports · 2021Article
- Toxic and Teratogenic Effects of Prenatal Alcohol Exposure on Fetal Development, Adolescence, and Adulthood.International journal of molecular sciences · 2021Review
- Review
- G9α-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice.Journal of cellular and molecular medicine · 2020Article
- Pulsed glucocorticoids enhance dystrophic muscle performance through epigenetic-metabolic reprogramming.JCI insight · 2019Observational
- Acetylation of H3K4, H3K9, and H3K27 mediated by p300 regulates the expression of GATA4 in cardiocytes.Genes & diseases · 2019Article
- Anacardic acid attenuates pressure-overload cardiac hypertrophy through inhibiting histone acetylases.Journal of cellular and molecular medicine · 2019Article
- Anticancer effects of plant derived Anacardic acid on human breast cancer MDA-MB-231 cells.American journal of translational research · 2018Article
- Novel detection of post-translational modifications in human monocyte-derived dendritic cells after chronic alcohol exposure: Role of inflammation regulator H4K12ac.Scientific reports · 2017Article
- Anacardic acid induces cell apoptosis of prostatic cancer through autophagy by ER stress/DAPK3/Akt signaling pathway.Oncology reports · 2017Article
- Histone 3 modifications and blood pressure in the Beijing Truck Driver Air Pollution Study.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2017Article
- Islet-1 induces the differentiation of mesenchymal stem cells into cardiomyocyte-like cells through the regulation of Gcn5 and DNMT-1.Molecular medicine reports · 2017Article
- Review
- Inhibition of histone acetylation by curcumin reduces alcohol-induced fetal cardiac apoptosis.Journal of biomedical science · 2017Article
- Review
- Histone modifications interact with DNA methylation at the GATA4 promoter during differentiation of mesenchymal stem cells into cardiomyocyte-like cells.Cell proliferation · 2016Article
- Epigenetic Mechanisms in Developmental Alcohol-Induced Neurobehavioral Deficits.Brain sciences · 2016Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiovascular malformations can be caused by abnormalities in Gata4 expression during fetal development. In a previous study, we demonstrated that ethanol exposure could lead to histone hyperacetylation and Gata4 over-expression in fetal mouse hearts. However, the potential mechanisms of histone hyperacetylation and Gata4 over-expression induced by ethanol remain unclear. METHODS AND
resultsPregnant mice were gavaged with ethanol or saline. Fetal mouse hearts were collected for analysis. The results of ethanol fed groups showed that global HAT activity was unusually high in the hearts of fetal mice while global HDAC activity remained unchanged. Binding of P300, CBP, PCAF, SRC1, but not GCN5, were increased on the Gata4 promoter relative to the saline treated group. Increased acetylation of H3K9 and increased mRNA expression of Gata4, α-MHC, cTnT were observed in these hearts. Treatment with the pan-histone acetylase inhibitor, anacardic acid, reduced the binding of P300, PCAF to the Gata4 promoter and reversed H3K9 hyperacetylation in the presence of ethanol. Interestingly, anacardic acid attenuated over-expression of Gata4, α-MHC and cTnT in fetal mouse hearts exposed to ethanol.
conclusionsOur results suggest that P300 and PCAF may be critical regulatory factors that mediate Gata4 over-expression induced by ethanol exposure. Alternatively, P300, PCAF and Gata4 may coordinate over-expression of cardiac downstream genes in mouse hearts exposed to ethanol. Anacardic acid may thus protect against ethanol-induced Gata4, α-MHC, cTnT over-expression by inhibiting the binding of P300 and PCAF to the promoter region of these genes.
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