Abstract：
:Maternal nicotine exposure causes alteration of gene expression and cardiovascular programming. The discovery of nicotine-medicated regulation in cardiogenesis is of major importance for the study of cardiac defects. The present study investigated the effect of nicotine on cardiac gene expression and epigenetic regulation during myocardial differentiation. Persistent nicotine exposure selectively inhibited expression of two cardiac genes, Tbx5 and Gata4, by promoter DNA hypermethylation. The nicotine-induced suppression on cardiac differentiation was restored by general nicotinic acetylcholine receptor inhibition. Consistent results of Tbx5 and Gata4 gene suppression and cardiac function impairment with decreased left ventricular ejection fraction were obtained from in vivo studies in offspring. Our results present a direct repressive effect of nicotine on myocardial differentiation by regulating cardiac gene suppression via promoter DNA hypermethylation, contributing to the etiology of smoking-associated cardiac defects.
journal_name
Stem Cell Reportsjournal_title
Stem cell reportsauthors
Jiang XY,Feng YL,Ye LT,Li XH,Feng J,Zhang MZ,Shelat HS,Wassler M,Li Y,Geng YJ,Yu XYdoi
10.1016/j.stemcr.2016.12.016subject
Has Abstractpub_date
2017-02-14 00:00:00pages
290-304issue
2issn
2213-6711pii
S2213-6711(16)30306-Xjournal_volume
8pub_type
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