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Placental gene expression in intestinal nematode-infected and protein-deficient mice

ABSTRACT: Protein deficiency and intestinal parasite infection during pregnancy impair fetal growth through passage of signals from the maternal environment which signal impairment of fetal growth. The placenta is an important regulator of the transfer of these signals through differential expression of key placental genes. We used microarrays to examine placental gene expression responses to maternal protein deficiency (6% vs. 24% protein) and Heligmosomoides bakeri infection.

ORGANISM(S): Mus musculus

PROVIDER: GSE57115 | GEO | 2015/09/09

SECONDARY ACCESSION(S): PRJNA245451

REPOSITORIES: GEO

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Placental gene expression in intestinal nematode-infected and protein-deficient mice

Project description:Protein deficiency and intestinal parasite infection during pregnancy impair fetal growth through passage of signals from the maternal environment which signal impairment of fetal growth. The placenta is an important regulator of the transfer of these signals through differential expression of key placental genes. We used microarrays to examine placental gene expression responses to maternal protein deficiency (6% vs. 24% protein) and Heligmosomoides bakeri infection. 2x2 factorial.

2015-09-09 | E-GEOD-57115 | biostudies-arrayexpress

Differential expression of genes in fetal brain as a consequence of maternal protein deficiency and nematode infection

Project description:Maternal dietary protein deficiency and nematode infection during early pregnancy have negative impacts on both maternal placental gene expression and fetal growth in the mouse. Here we used next-generation RNA sequencing to test our hypothesis that maternal protein deficiency and/or nematode infection also alter the expression of genes in the developing fetal brain. Outbred pregnant CD1 mice were used in a 2x2 design with two levels of dietary protein (24% and 6%) and two levels of infection (repeated sham and Heligmosomoides bakeri beginning at gestation day 5). Pregnant dams were euthanized on gestation day 18 to harvest the whole fetal brain. Four fetal brains from each treatment group were analyzed using RNA Hi-seq sequencing and the differential expression of genes was determined by edgeR package using NetworkAnalyst. In response to maternal H. bakeri infection, 96 genes (88 up-regulated and 8 down-regulated) were differentially expressed in the fetal brain. Differentially expressed genes were involved in metabolic processes, developmental processes and immune system according to the PANTHER classification system. Among the important biological functions identified, several upregulated genes have known neurological functions including neurodevelopment (Gdf15, Ing4), neural differentiation (miRNA let-7), synaptic plasticity (via suppression of NF-κβ), neuro-inflammation (S100A8, S100A9) and glucose metabolism (Tnnt1, Atf3). However, in response to maternal protein deficiency, brain specific serine protease (Prss22) was the only upregulated gene and only one gene (Dynlt1a dynein light chain) responded to the interaction of maternal nematode infection and PD. In conclusion, maternal exposure to GI nematode infection from day 5 to 18 of pregnancy may influence developmental programming of the fetal brain.

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Maternal Nematode Infection Up-regulates Expression of Genes Associated with Long-Term Potentiation in Brains of Uninfected Pups

Project description:Pregnant mice were infected with Heligmosomoides bakeri nematode on gestation day 7, 12 and 17 and on postnatal day 3. Pup brain were collected on postnatal day 2 and 7 and sequenced in illumina HiSeq4000 PE100 sequencing lane

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [Bulk RNA-seq]

Project description:Enteric helminths form intimate physical connections with the intestinal epithelium, yet their ability to directly alter epithelial stem cell fate has not been resolved. Here we demonstrate that infection of mice with the symbiotic parasite Heligmosomoides polygyrus bakeri (Hpb), reprograms the intestinal epithelium into a fetal-like state marked by the emergence of Clusterin-expressing revival stem cells (revSCs). Organoid-based studies using parasite-derived excretory/secretory products reveal that Hpb-mediated revSC generation occurs independent of host-derived immune signals and inhibits type 2 cytokine-driven differentiation of secretory epithelial lineages that promote their expulsion. Reciprocally, type 2 cytokine signals limit revSC differentiation and, consequently, Hpb fitness indicating that helminths compete with their host for control of the intestinal stem cell niche to promote continuation of their life cycle.

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [scRNA-seq]

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Extracellular vesicles from Heligmosomoides bakeri and Trichuris muris contain distinct small RNAs

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Heligmosomoides bakeri

Project description:Heligmosomoides bakeri overview

| PRJNA902479 | ENA

Transcription profiling of mouse placenta to determine the relative effects of maternal and fetal genotype on the placental transcriptome at E18.5

Project description:The placenta plays a crucial role in the normal growth and development in mammals by serving as an interface for nutrients, respiratory gases and physiological signals between the mother and fetus. Here we use a novel embryo transfer system in mice to identify the major physiological pathways in the placenta that are principally influenced by altered maternal environment. Embryos of identical genotype were transferred at the one cell stage into surrogate mothers either of the same strain or from a different strain. We analyzed the relative effects of maternal and fetal genotype on fetal weight, placental weight and the placental transcriptome at E18.5. The results show that maternal genotype overrides fetal genotype as the principal regulator of fetal weight (p<0.0001). Microarray analysis of the transcriptome in placentas revealed that a small fraction (0.25%) of placental genes are specifically regulated by maternal genotype (p<0.05, FDR<0.10). Pathway analysis of these genes using the programs Gene Ontology and MetaCore from GeneGO inc. revealed highest statistical significance in signaling pathways that regulate cell growth and lipid metabolism. These results provide a mechanistic understanding of important molecular pathways involved in maternal regulation of fetal growth and development.

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Maternal Influenza A Virus Infection Restricts Fetal and Placental Growth and Adversely Affects the Fetal Thymic Transcriptome

Project description:Maternal influenza A viral infections in humans are associated with low birth weight, increased risk of pre-term birth, stillbirth and congenital defects. To examine the effect of maternal influenza virus infection on placental and fetal growth, pregnant C57BL/6 mice were inoculated intranasally with influenza A virus A/CA/07/2009 pandemic H1N1 or PBS at E3.5, E7.5 or E12.5, and the placentae and fetuses collecgted and weighed at E18.5. Fetal thymuses were pooled from each litter. Placentae were examined histologically, stained by IHC for CD34 and vascular channels quantified. RNA from E7.5 and E12.5 placentae and E7.5 fetal thymuses was subjected to RNA sequencing and pathway analysis. Placental weights were decreased in litters inoculated with influenza at E3.5 and E7.5. Placentae from E7.5 and E12.5 inoculated litters exhibited decreased labyrinth development and transmembrane protein 150A gene was upregulated in E7.5 placentae. Fetal weights were decreased in litters inoculated at E7.5 and E12.5 compared to controls. RNA sequencing of E7.5 thymuses indicated that 957 genes were downregulated 2-fold including Mal, which is associated with Toll-like receptor signaling and T cell differentiation. There were 28 upregulated genes. It is concluded that maternal influenza A virus infection impairs fetal thymic gene expression as well as restricting placental and fetal growth.

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Proteomic And Phosphoproteomic Study Of Placenta And Fetal Liver In Mice With Diet-Induced Obesity

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2019-01-24 | PXD011722 | Pride

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