Fetal blood transcriptome in maternal anti-fetal rejection
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE28387 | GEO | 2012/04/01
SECONDARY ACCESSION(S): PRJNA139197
REPOSITORIES: GEO
Similar Datasets
Project description:Both the fetus and the mother who are involved in maternal anti-fetal rejection during pregnancy show distinct alterations in the peripheral blood transcriptome Total RNA isolated from umbilical cord blood and maternal blood was compared between cases without (Normal) and with maternal anti-fetal rejection (FIRS2) using whole genome DASL assay.
2012-03-31 | E-GEOD-28387 | biostudies-arrayexpress
Project description:Pregnancy is a time of extreme metabolic demand that requires coordinated adaptations between mother and fetus. To determine the contributions of maternal and fetal metabolism to metabolic plasticity during gestation, mice with a liver-specific Carnitine Palmitoyltransferase-2 knockout mice (Cpt2-/-), or Pparα KO mice were subjected to late-gestation nutrient stress, a 24hr fast from E16.5 to E17.5. The fetal response to maternal fasting was dominated by maternal lipid metabolism as the loss of maternal hepatic fatty acid oxidation or Pparα signaling accelerated fetal liver transcriptional programing. These data show that maternal nutritional environment is a major driver of perinatal metabolic programing and plasticity.
2019-09-20 | GSE129368 | GEO
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.
2024-06-13 | PXD039402 | Pride
Project description:Activation of the maternal immune system during pregnancy affects fetal development, which can increase in postnatal susceptibility to a 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, essentials 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 acute maternal lung inflammation across time in maternal and fetal organs, using a combination of omics, imaging and integrative computational analyses. We found that the placenta, unlike other maternal organs, did not react by a typical innate immune response, but instead induced genes associated with increased tissue integrity, likely to prevent fetal exposure to potential infections, and simultaneously reduced expression of growth-associated genes. Subsequently, a return to homeostasis was observed, with heightened expression of biosynthesis and endoplasmic reticulum (ER) stress genes. These responses likely protect 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) carrying metabolites, including triglyceride and phosphatidylcholine. Notably, DHA is crucial for fetal brain development. 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 integrated temporal and systemic response to LPS in lungs across maternal and fetal organs
2024-02-01 | GSE224116 | GEO
Project description:The placenta acts as an interface between the mother and fetus, regulating nutrient transport and secreting hormones which impact maternal metabolism. Complications during pregnancy, such as placental endocrine malfunction, programme offspring to develop metabolic disease during adulthood, in part via changes in gene expression in critical metabolic organs, such as the liver, during fetal development. Placental endocrine malfunction was induced via the misexpression of two imprinted genes (Igf2 and H19) exclusively in the endocrine zone of the mouse placenta, to study the consequences this has on fetal hepatic gene expression.
2023-11-30 | E-MTAB-11457 | biostudies-arrayexpress
Project description:During pregnancy, cells from each fetus travel into the maternal circulation and organs, resulting in the development of microchimerism. Identification of the cell types in this microchimeric population would permit better understanding of possible mechanisms by which they affect maternal health. However, comprehensive analysis of fetal cells has been hampered by their rarity. In this study, we sought to overcome this obstacle by combining flow cytometry with multidimensional gene expression microarray analysis of fetal cells isolated from the murine maternal lung during late pregnancy. Fetal cells were collected from the lungs of pregnant female mice. cDNA was amplified and hybridized to gene expression microarrays. The resulting fetal cell core transcriptome was interrogated using multiple methods including Ingenuity Pathway Analysis, the BioGPS gene expression database, principal component analysis, the Eurexpress gene expression atlas and primary literature. Here we report that small numbers of fetal cells can be flow sorted from the maternal lung, facilitating discovery-driven gene expression analysis. We additionally show that gene expression data can provide functional information about the fetal cells. Our results suggest that fetal cells in the murine maternal lung are a mixed population, consisting of trophoblasts, mesenchymal stem cells and cells of the immune system. The detection of trophoblasts and immune cells in the maternal lung may facilitate future mechanistic studies related to the development of immune tolerance and pregnancy-related complications, such as preeclampsia. Furthermore, the presence and persistence of mesenchymal stem cells in maternal organs may have implications for long-term postpartum maternal health. Comprehensive gene expression microarray analysis of fetal cells isolated from the pregnant murine maternal lung. Seven individual replicates were performed.
2012-05-30 | E-GEOD-38188 | biostudies-arrayexpress
Project description:Growing evidence supports the hypothesis that the in utero environment can have profound implications for fetal development and for offspring health in later life. Current theory suggests that conditions experienced in utero prepare, or ‘programme’, the fetus for its anticipated post-natal environment. The mechanisms responsible for these programming events are poorly understood but are likely to involve gene expression changes. Folate is essential for normal fetal development and inadequate maternal folate supply during pregnancy has long term adverse effects on the offspring. We tested the hypothesis that inadequate folate supply during pregnancy alters offspring programming through altered gene expression. Female C57BL/6J mice were fed diets containing 2 mg folic acid/kg or 0.4 mg folic acid/kg for 4 weeks before mating and throughout pregnancy. At 17.5 day gestation, genome-wide gene expression in fetal liver and placenta of male offspring was measured by microarray analysis. In the fetal liver, 989 genes (555 up-regulated, 434 down-regulated) were expressed differentially in response to maternal folate depletion, with 460 genes expressed differentially (250 up-regulated, 255 down-regulated) in the placenta. Only 25 differentially expressed genes were common between organs, revealing that maternal folate intake during pregnancy influences fetal gene expression in a highly organ specific manner which, we propose, reflects prioritised protection of essential organ-specific functions.
2016-06-14 | E-MTAB-3940 | biostudies-arrayexpress
Project description:We investigated how late fetal liver (FL) mouse hematopoieitic stem and progenitor cells (HSPC) respond to inflammation, with the hypothesis that deficits in engagement of emergency myelopoiesis (EM) pathways could limit neutrophil output and contribute to perinatal neutropenia, ultimately explaining the susceptibility of neonates to inflammation and infection. We show that fetal HSPCs are biased toward erythroid and lymphoid cell production at steady state and fail to mount classical EM responses in vivo. Despite being capable of responding to EM-inducing stimuli in vitro, we find that maternal factors like interleukin-10 (IL-10) restrict fetal HSPCs from activating EM pathways in utero. Accordingly, we find that loss of maternal IL-10 restores EM activation in fetal HSPCs but at a cost of premature parturition. These results reveal the evolutionary trade-off inherent in maternal anti-inflammatory responses that maintain pregnancy but render the fetus susceptible to infection.
2024-02-29 | GSE240914 | GEO
Project description:We investigated how late fetal liver (FL) mouse hematopoieitic stem and progenitor cells (HSPC) respond to inflammation, with the hypothesis that deficits in engagement of emergency myelopoiesis (EM) pathways could limit neutrophil output and contribute to perinatal neutropenia, ultimately explaining the susceptibility of neonates to inflammation and infection. We show that fetal HSPCs are biased toward erythroid and lymphoid cell production at steady state and fail to mount classical EM responses in vivo. Despite being capable of responding to EM-inducing stimuli in vitro, we find that maternal factors like interleukin-10 (IL-10) restrict fetal HSPCs from activating EM pathways in utero. Accordingly, we find that loss of maternal IL-10 restores EM activation in fetal HSPCs but at a cost of premature parturition. These results reveal the evolutionary trade-off inherent in maternal anti-inflammatory responses that maintain pregnancy but render the fetus susceptible to infection.
2024-02-29 | GSE240913 | GEO
Project description:We investigated how late fetal liver (FL) mouse hematopoieitic stem and progenitor cells (HSPC) respond to inflammation, with the hypothesis that deficits in engagement of emergency myelopoiesis (EM) pathways could limit neutrophil output and contribute to perinatal neutropenia, ultimately explaining the susceptibility of neonates to inflammation and infection. We show that fetal HSPCs are biased toward erythroid and lymphoid cell production at steady state and fail to mount classical EM responses in vivo. Despite being capable of responding to EM-inducing stimuli in vitro, we find that maternal factors like interleukin-10 (IL-10) restrict fetal HSPCs from activating EM pathways in utero. Accordingly, we find that loss of maternal IL-10 restores EM activation in fetal HSPCs but at a cost of premature parturition. These results reveal the evolutionary trade-off inherent in maternal anti-inflammatory responses that maintain pregnancy but render the fetus susceptible to infection.
2024-02-29 | GSE240912 | GEO