Similar Datasets
Project description:Immune molecules, including cytokines, chemokines, and their cognate receptors, are developmentally regulated in the brain and dynamically expressed in the context of neurodevelopmental and neuropsychiatric disease. Here, we employed highly multiplexed in situ spatial transcriptomics to map the expression of major immune ligands and receptors in the developing mouse brain during mid and late gestation. Given the importance of the maternal environment in shaping fetal neurodevelopment, we also determined how the embryonic neuroimmune landscape was altered after maternal immune and microbiome perturbations, with notable sex-specific patterns. We discovered significant changes in the expression of the CXCL12/CXCR7 chemokine network after maternal immune activation and maternal microbiome depletion, suggesting an underlying mechanism for corticogenesis abnormalities. This resource underscores how the maternal environment programs the precise regulation of immune molecules in the developing brain, highlighting sex-specific disease vulnerability.
2025-06-01 | GSE269617 | GEO
Project description:The Maternal Gut-Immune Axis Programs the Neuroimmune Landscape of the Developing Brain [snATAC-seq]
| PRJNA1154254 | ENA
Project description:The Maternal Gut-Immune Axis Programs the Neuroimmune Landscape of the Developing Brain
| PRJNA1123009 | ENA
Project description:This study used droplet-based snATAC-seq to profile the chromatin accessibility landscape of 91,922 nuclei in the mouse cerebellum across eleven developmental stages, from the beginning of neurogenesis (e10.5) till adulthood (P63). The study included two biological replicates per stage, one from each sex. Cerebelli were dissected as whole or in two halves, nuclei were extracted and profiled using 10x single-cell ATAC reagent kit (v1.0) and a Chromium controller. Libraries were sequenced using paired-reads on Illumina NextSeq 550 and initial data processing was performed using Cellranger ATAC (1.1).
2021-09-07 | E-MTAB-9765 | biostudies-arrayexpress
Project description:Maternal diabetes is a well-known risk factor for birth defects, such as heart defects and neural tube defects. The causative molecular mechanisms in the developing embryo are currently unknown, and the pathogenesis of developmental abnormalities during diabetic pregnancy is not well understood. We hypothesized that the developmental defects are due to alterations in critical developmental pathways, possibly as a result of altered gene expression. We here report results from gene expression profiling of exposed embryos from a mouse diabetes model.In comparison to normal embryos at mid-gestation, we find significantly altered gene expression levels in diabetes-exposed embryos. Independent validation of altered expression was obtained by quantitative Real Time Polymerase Chain Reaction. Sequence motifs in the promoters of diabetes-affected genes suggest potential binding of transcription factors that are involved in responses to oxidative stress and/or to hypoxia, two conditions known to be associated with diabetic pregnancies. Functional annotation shows that a sixth of the de-regulated genes have known developmental phenotypes in mouse mutants. Over 30% of the genes we have identified encode transcription factors and chromatin modifying proteins or components of signaling pathways that impinge on transcription.Exposure to maternal diabetes during pregnancy alters transcriptional profiles in the developing embryo. The enrichment, within the set of de-regulated genes, of those encoding transcriptional regulatory molecules provides support for the hypothesis that maternal diabetes affects specific developmental programs.
| S-EPMC2715936 | biostudies-literature
Project description:We profiled the epigenetic landscape of the developing mouse embryo across three ages (E12.5, E13.5, and E15.5) using single nuclei processed with 10X Genomics's Single Cell ATAC platform.
2022-11-03 | GSE214988 | GEO
Project description:We profiled the epigenetic landscape of the developing mouse embryo across three ages (E12.5, E13.5, and E15.5) using fresh frozen tissue sections processed with 10X Genomics's OMNI ATAC, which allows to record regions of open chromatin while retaining spatial resolution.
2022-11-03 | GSE214986 | GEO
Project description:Chronic early life stress (ELS) potently impacts the developing central nervous and immune systems and is associated with the onset of gastrointestinal disease in humans. Though the gut-brain axis is appreciated to be a major target of the stress response, the underlying mechanisms linking ELS to gut dysfunction later in life is incompletely understood. Zebrafish are a powerful model validated for stress research and have emerged as an important tool in delineating neuroimmune mechanisms in the developing gut. Here, we developed a novel model of ELS and utilized a comparative transcriptomics approach to assess how chronic ELS modulated expression of neuroimmune genes in the developing gut and brain. Zebrafish exposed to ELS throughout larval development exhibited anxiety-like behavior and altered expression of neuroimmune genes in a time- and tissue-dependent manner. Further, the altered gut neuroimmune profile, which included increased expression of genes associated with neuronal modulation, correlated with a reduction in enteric neuronal density and delayed gut transit. Together, these findings provide insights into the mechanisms linking ELS with gastrointestinal dysfunction and highlight the zebrafish model organism as a valuable tool in uncovering how "the body keeps the score."
| S-EPMC10336164 | biostudies-literature
Project description:One of the key proposed agents of fetal programming is exposure to maternal glucocorticoids. Experimental animal studies provide evidence that prenatal exposure to elevated maternal glucocorticoids has consequences for hypothalamic-pituitary-adrenal (HPA) axis functioning in the offspring. There are very few direct tests of maternal glucocorticoids, such as cortisol, during human pregnancy and associations with infant cortisol reactivity. The current study examined the link between maternal prenatal cortisol trajectories and infant cortisol reactivity to the pain of inoculation in a sample of 152 mother-infant (47.4% girls) pairs. The results from the current study provide insight into fetal programming of the infant HPA axis, demonstrating that elevated prenatal maternal cortisol is associated with a larger infant cortisol response to challenge at both 6 and 12 months of age.
| S-EPMC9743740 | biostudies-literature
Project description:Exposure to maternal diabetes during pregnancy alters transcriptional profiles in the developing embryo. The enrichment, within the set of de-regulated genes, of those encoding transcriptional regulatory molecules provides support for the hypothesis that maternal diabetes affects specific developmental programs. We compared E10.5 cntrol embryos to E10.5 embryos from diabetic pregnancies in the FVB mouse strain. Diabetes was induced in 7-9 week old female FVB mice by streptozotocin. Dams whose blood glucose levels exceeded 250 mg/dl were set up for mating. Embryos were dissected at E10.5 and total RNA was isolated. Equal amounts of RNA prepared from 3 individual embryos were pooled into one sample; each embryo was from a different pregnancy. Three pools were constructed for a total of nine embryos from diabetic pregnancies, and independently three pools for control embryos.
2012-09-25 | E-GEOD-41095 | biostudies-arrayexpress