Center for Genomics, School of Medicine, Loma Linda University, Loma Linda, CA, 92350, USA.
Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, 92350, USA.
Sci Data. 2019 Oct 29;6(1):238. doi: 10.1038/s41597-019-0253-9.
The molecular mechanism of antenatal hypoxia impacting on fetal heart development and elevated risk of heart disease of adult offspring is poorly understood. We present a dataset integrating DNA methylome and transcriptome analyses of antenatal hypoxia affecting rat fetal and adult offspring hearts to understand hypoxia-mediated epigenomic reprogramming of the heart development. We showed that antenatal hypoxia not only induced DNA methylomic and transcriptomic changes in the fetal hearts, but also had a delayed and lasting effect on the adult offspring hearts. Of interest, antenatal hypoxia induced opposite changes in DNA methylation patterns in fetal and adult hearts, with a hypermethylation in the fetus and a hypomethylation in the adult. An extensive preprocessing, quality assessment, and downstream data analyses were performed on the genomic dataset so that the research community may take advantage of the public resource. These dataset could be exploited as a comprehensive resource for understanding fetal hypoxia-mediated epigenetic reprogramming in the heart development and further developmental programming of heart vulnerability to disease later in life.Figshare doi: https://doi.org/10.6084/m9.figshare.9948572.
产前缺氧影响胎儿心脏发育并增加成年后代患心脏病风险的分子机制尚不清楚。我们提供了一个整合了产前缺氧影响大鼠胎儿和成年后代心脏的 DNA 甲基化组和转录组分析的数据集，以了解缺氧对心脏发育的表观遗传重编程。结果表明，产前缺氧不仅导致胎儿心脏的 DNA 甲基化组和转录组发生变化，而且对成年后代心脏也有延迟和持久的影响。有趣的是，产前缺氧在胎儿和成年心脏中诱导了 DNA 甲基化模式的相反变化，胎儿中呈现超甲基化，而成年中呈现低甲基化。对基因组数据集进行了广泛的预处理、质量评估和下游数据分析，以便研究界可以利用公共资源。这些数据集可以作为理解胎儿缺氧介导的心脏发育中表观遗传重编程以及进一步发育编程的综合资源，以了解心脏对疾病的易感性。Figshare doi：https://doi.org/10.6084/m9.figshare.9948572.
