G9α-dependent histone H3K9me3 hypomethylation promotes overexpression of cardiomyogenesis-related genes in foetal mice.

摘要: Alcohol consumption during pregnancy can cause foetal alcohol syndrome and congenital heart disease. Nonetheless, the underlying mechanism of alcohol-induced cardiac dysplasia remains unknown. We previously reported that exposure abnormal expression cardiomyogenesis-related genes, histone H3K9me3 hypomethylation was observed in alcohol-treated mouse heart. Hence, an imbalance methylation may be involved dysplasia. In this study, we investigated involvement G9α methyltransferase vivo vitro using tissues mice primary cardiomyocytes neonatal mice. Western blotting revealed caused by altering cardiomyocytes. Moreover, overexpression genes (MEF2C, Cx43, ANP β-MHC) alcohol-exposed Additionally, demonstrated directly interacted with altered its methylation. Notably, did not down-regulate after suppression short hairpin RNA cardiomyocytes, preventing MEF2C, β-MHC overexpression. These findings suggest methyltransferase-mediated plays a critical role pregnancy. Therefore, intervention target for