Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq of human fetal liver in fetuses exposed to cigarette smoke in utero compared to non-exposed controls

ABSTRACT: In utero smoke exposure has adverse consequences for the child, including premature delivery, smaller birth weight and predisposition to disease later in life. The fetal liver has major detoxifying roles in addition to orchestrating the function of multiple organ systems. Maternal smoking increases the fetal toxin burden, and is expected to cause changes in the human fetal liver physiology likely contributing to disease and disease predisposition. In this project the transcriptional response in fetal liver tissue was analysed in relation to maternal smoke exposure, fetal sex and gestational age. Total RNA, protein and DNA were consecutively extracted from the same liver biopsy of electively terminated second trimester fetal livers. Proteomic analyses on the protein fraction were performed to allow for an integrated analysis of both the transcriptional and translational changes.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER:

PROVIDER: E-MTAB-6103 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP104556

REPOSITORIES: biostudies-arrayexpress

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Project description:Activation of the maternal immune system during pregnancy can fetal development, which can lead to postnatal susceptibility to a wide range of diseases, including cardiovascular, metabolic and psychiatric disorders. During maternal immune activation (MIA), the maternal body must balance its ressources between mounting an immune response and investing resources into continued metabolism and growth : both essential for survival of the fetus and a successful pregnancy. How the placenta responds to MIA over time and how it can protect the fetus is not well understood, and neither are the fetal consequences of MIA. Here, we characterised the response to an induced acute inflammation in maternal lungs over time across maternal and fetal organs, using a combination of omics-methods, imaging and integrative computational analysis. We found that the placenta, unlike other maternal organs, did not react by inducing a typical inflammatory response, but instead initially induced genes associated to strengthen tissue integrity and simultaneously reduced growth to prevent exposure to potential infections. Afterwards, a return to homeostasis was observed, with heightened biosynthesis and expression of endoplasmic reticulum (ER) stress genes. This mechanism likely protects the fetus from inflammation, as we observed no immune response in the fetal liver transcriptome. Instead, we observed metabolic adaptations in the fetus, including a release of docosahexaenoic acid (DHA) Notably, DHA has a crucial function for fetal brain development , and levels of triglyceride and phosphatidylcholine lipids that are necessary for transportation of DHA to the brain were also increased. This metabolic response is likely a combination of the placental MIA response and temporary maternal fasting, caused by MIA-induced fever and lack of nutrient intake. Our study shows, for the first time, the temporal and systemic response to MIA in lungs across maternal and fetal organs.

Dataset Information

RNA-seq of human fetal liver in fetuses exposed to cigarette smoke in utero compared to non-exposed controls

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