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Background  Cardiovascular 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 Results  Pregnant 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.    Conclusions  Our 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.

plos one

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