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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

ABSTRACT: Identification of factors that control ifn responses during pregnancy

ORGANISM(S): Homo sapiens

PROVIDER: GSE143429 | GEO | 2021/01/14

REPOSITORIES: GEO

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-14 | GSE143432 | GEO

GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

Project description:Inhibition of GPER1 in pregnant mice significantly alters inflammation and angiogenesis in the placenta, but does not significantly impact the lung

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [RNAseq]

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GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

Project description:GPER1 inhibits placental type I IFN responses to preserve fetal health during maternal infection [GECKOscreen]

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GPER1 is required to protect fetal health from maternal inflammation.

Project description:Type I interferon (IFN) signaling in fetal tissues causes developmental abnormalities and fetal demise. Although pathogens that infect fetal tissues can induce birth defects through the local production of type I IFN, it remains unknown why systemic IFN generated during maternal infections only rarely causes fetal developmental defects. Here, we report that activation of the guanine nucleotide-binding protein-coupled estrogen receptor 1 (GPER1) during pregnancy is both necessary and sufficient to suppress IFN signaling and does so disproportionately in reproductive and fetal tissues. Inactivation of GPER1 in mice halted fetal development and promoted fetal demise, but only in the context of maternal inflammation. Thus, GPER1 is a central regulator of IFN signaling during pregnancy that allows dynamic antiviral responses in maternal tissues while also preserving fetal health.

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Maternal cadmium, placental PCDHAC1, and fetal development.

Project description:Cadmium (Cd) is a ubiquitous environmental contaminant implicated as a developmental toxicant, yet the underlying mechanisms that confer this toxicity are unknown. Mother-infant pairs from a Rhode Island birth cohort were investigated for the potential effects of maternal Cd exposure on fetal growth, and the possible role of the PCDHAC1 gene on this association. Mothers with higher toenail Cd concentrations were at increased odds of giving birth to an infant that was small for gestational age or with a decreased head circumference. These associations were strongest amongst those with low levels of DNA methylation in the promoter region of placental PCDHAC1. Further, we found placental PCDHAC1 expression to be inversely associated with maternal Cd, and PCDHAC1 expression positively associated with fetal growth. Our findings suggest that maternal Cd affects fetal growth even at very low concentrations, and some of these effects may be due to the differential expression of PCDHAC1.

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The significance of the placental genome and methylome in fetal and maternal health.

Project description:The placenta is a crucial organ for supporting a healthy pregnancy, and defective development or function of the placenta is implicated in a number of complications of pregnancy that affect both maternal and fetal health, including maternal preeclampsia, fetal growth restriction, and spontaneous preterm birth. In this review, we highlight the role of the placental genome in mediating fetal and maternal health by discussing the impact of a variety of genetic alterations, from large whole-chromosome aneuploidies to single-nucleotide variants, on placental development and function. We also discuss the placental methylome in relation to its potential applications for refining diagnosis, predicting pathology, and identifying genetic variants with potential functional significance. We conclude that understanding the influence of the placental genome on common placental-mediated pathologies is critical to improving perinatal health outcomes.

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IFN-kappa inhibits HPV31 transcription by inducing Sp100 proteins

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2015-11-04 | E-GEOD-74658 | biostudies-arrayexpress

Hypertension and maternal-fetal conflict during placental malaria.

Project description:BackgroundMalaria and hypertension are major causes of maternal mortality in tropical countries, especially during first pregnancies, but evidence for a relationship between these syndromes is contradictory.Methods and findingsIn a cross-sectional survey of Tanzanian parturients, the rate of hypertension was similar in placental malaria (PM)-positive (11/85 = 13%) and PM-negative (73/602 = 12%) individuals. However, we found that PM was associated with hypertension in first-time mothers aged 18-20 y but not other mothers. Hypertension was also associated with histologic features of chronic malaria, which is common in first-time mothers. Levels of soluble vascular endothelial growth factor receptor 1 (sVEGFR1), a preeclampsia biomarker, were elevated in first-time mothers with either PM, hypertension, or both, but levels were not elevated in other mothers with these conditions. In first-time mothers with PM, the inflammatory mediator vascular endothelial growth factor (VEGF) was localized to maternal macrophages in the placenta, while sVEGFR1, its soluble inhibitor, was localized to the fetal trophoblast.ConclusionsThe data suggest that maternal-fetal conflict involving the VEGF pathway occurs during PM, and that sVEGFR1 may be involved in the relationship between chronic PM and hypertension in first-time mothers. Because placental inflammation causes poor fetal outcomes, we hypothesize that fetal mechanisms that promote sVEGFR1 expression may be under selective pressure during first pregnancies in malaria-endemic areas.

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