全氟辛烷
胚胎干细胞
线粒体
细胞生物学
毒性
发育毒性
生物
细胞凋亡
祖细胞
氧化磷酸化
干细胞
化学
生物化学
基因
遗传学
磺酸盐
怀孕
妊娠期
有机化学
钠
作者
Min Qiu,Jing Chen,Mingqin Liu,Zhiqiang Nie,Miao-La Ke,Guang‐Hui Dong,Haishan Zhao,Chengbin Zhou,Heng Zeng,Biaochuan He,Jimei Chen,Jian Zhuang,Xiaohong Li,Yanqiu Ou
标识
DOI:10.1016/j.ecoenv.2024.115945
摘要
Perfluorooctane sulfonate (PFOS), an endocrine-disrupting chemical pollutant, affects embryonic heart development; however, the mechanisms underlying its toxicity have not been fully elucidated. Here, Single-cell RNA sequencing (scRNA-seq) was used to investigate the overall effects of PFOS on myocardial differentiation from human embryonic stem cells (hESCs). Additionally, apoptosis, mitochondrial membrane potential, and ATP assays were performed. Downregulated cardiogenesis-related genes and inhibited cardiac differentiation were observed after PFOS exposure in vitro. The percentages of cardiomyocyte and cardiac progenitor cell clusters decreased significantly following exposure to PFOS, while the proportion of primitive endoderm cell was increased in PFOS group. Moreover, PFOS inhibited myocardial differentiation and blocked cellular development at the early- and middle-stage. A Gene Ontology analysis and pseudo-time trajectory illustrated that PFOS disturbed multiple processes related to cardiogenesis and oxidative phosphorylation in the mitochondria. Furthermore, PFOS decreased mitochondrial membrane potential and induced apoptosis. These results offer meaningful insights into the cardiogenic toxicity of PFOS exposure during heart formation as well as the adverse effects of PFOS on mitochondria.
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