期刊
STEM CELL REPORTS
卷 8, 期 2, 页码 290-304出版社
CELL PRESS
DOI: 10.1016/j.stemcr.2016.12.016
关键词
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资金
- National Natural Science Foundation of China [81120108003, 81330007, U1601227]
- Scientific and Technological Key Projects of Guangdong Province [2014A050503047, 2015B020225006]
- American Heart Association [0765149Y]
- MacDonald Foundation [10RDM009, 07RDM008]
- NIH [R01HL69509]
- Department of Defense [10117004]
- Guangzhou Government and Overseas Study Program of the Guangzhou Elite Project
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.
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