作者: Wei Cheng , Ren Zhou , Yan Feng , Yan Wang
DOI: 10.1016/J.TOX.2016.05.017
关键词: MEF2C 、 Embryonic stem cell 、 Sidestream smoke 、 Heart development 、 Bone morphogenetic protein 、 Anatomy 、 Histone H3 acetylation 、 Biology 、 Cell biology 、 Myosin 、 Myosin light-chain kinase
摘要: Epidemiology studies suggest that maternal smoking and passive have strongly resulted in the occurrence of congenital heart defects (CHD) offspring. Cigarette smoke (CS) can be divided into mainstream (MS) sidestream (SS); CS chemistry study indicates significant differences exist composition MS SS. Therefore, SS were suspected to process toxicity dissimilarly. However, much less was known about difference developmental effects induced by In current study, development mimicked mouse embryonic stem cells (ESCs) differentiation. After exposure, tracing bone morphogenetic protein (BMP)-Smad4 signalling pathway, interruption downstream gene expression observed, including Gata4, Mef2c Nkx2.5, as well myosin heavy chain light chain. Specifically, caused inhibition Gata4 expression, even at non-cytotoxic concentration. Further, SS-induced hypoacetylation promoter regions reflected orchestration CS-gene modulation-epigenetic regulation. Even though apoptosis ESC-derived cardiomyocytes, partial clearance with down-regulated these survive undergo further differentiation, which laid potential risk for abnormal development. These data uncovered between on preliminarily.