Neurobehavioral abnormalities following prenatal psychosocial stress are differentially modulated by maternal environment
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PROVIDER: PRJNA782567 | ENA |
REPOSITORIES: ENA
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Project description:The goal of this study was to compare transcriptional profiles of the amygdala from control and (PS) prenatally stressed male and female offspring to elucidate sex-specific molecular mechanisms underlying behavioral and neuroendocrine abnormalities observed after in-utero psychosocial stress exposure. Amygdalar mRNA profiles of 28 day old control and PS male and female mice were generated by preparing sequencing libraries using the NEBNext Ultr II Directional RNA Library Prep Kit for Illumina. After indexing, enrichment through 8 cycles of PCR, and passing initial quality control metrics, individually indexed and compatible libraries were proportionally pooled and sequenced using Nextseq 550 sequencer. The sequencing setting of single read 1 × 85 bp to generate ∼50 M reads per sample was used. Differentially expressed genes (DEGs) were analyzed using RUVseq and EdgeR. Results were validated via qPCR We find psychosocial PS results in the emergence of anxiety-like behaviors, an altered behavioral coping strategy to stress, and anhedonia in male and female offspring. Neuroendocrine abnormalities, evidenced by acute stress-induced HPA axis hyperactivity, are only observed in PS female offspring. Our RNA-seq analysis reveals these phenotypic changes in PS offspring to be associated with sex-specific disturbances in genes associated with synaptic transmission, including genes associated with glutamatergic and GABAergic signaling in PS males, and upregulation of DBH, known to regulate NE synthesis, in PS females. Our study represents one of the first detailed analysis of amygdalar transcriptomes generated by RNA-seq comparing control vs prenatally stressed offspring, identifying sex-specific changes in response to in-utero psychosocial stress exposure.
2022-02-08 | GSE189330 | GEO
Project description:we have conducted a comparative study of the different technologies available for the detection of chromosomal abnormalities in prenatal samples. Here we include results of the aCGH experiments this series is composed of internal controls plus a year-long (2009-2010) consecutive series of pregnant women with indication for prenatal screening of chromosomal abnormalities a pdf and txt version of the table with 'sample name' plus relevant sample characteristics, including chromosomal abnormalities identified in our work is provided as a supplementary file on the Series record (below).
2014-01-07 | E-GEOD-26654 | biostudies-arrayexpress
Project description:In the study presented here, microRNA expression was profiled in blood samples from mothers of children with autism, with known stress exposure during pregnancy. 2500 mature microRNAs were examined. Thirty-four maternal blood samples were examined in this study. Samples were divided into five groups based on maternal SERT genotypes (LL/LS/SS) and prenatal stress level (High/Low).
2021-07-02 | GSE179222 | GEO
Project description:we have conducted a comparative study of the different technologies available for the detection of chromosomal abnormalities in prenatal samples. Here we include results of the aCGH experiments
2014-01-07 | GSE26654 | GEO
Project description:Massively parallel sequencing of maternal cell-free DNA (cfDNA) is widely used to test fetal genetic abnormalities in non-invasive prenatal testing (NIPT). However, sequencing-based approaches are still of high cost. Building upon previous knowledge that placenta, the main source of fetal circulating DNA, is hypomethylated in comparison to maternal tissue counterparts of cfDNA, we propose that targeting either unmodified or 5-hydroxymethylated CG sites specifically enriches fetal genetic material and reduces numbers of required analytical sequencing reads thereby decreasing cost of a test.
2020-10-20 | GSE148964 | GEO
Project description:Objective: The study compared the incidence of aneuploidy and copy number variations (CNVs) in fetuses with increased nuchal translucency (NT) to those with clear indications for non-invasive prenatal screening (NIPS), aiming to evaluate the risk of routine aneuploidy (RA) and pathogenic submicroscopic abnormalities and the potential use of NIPS for fetuses with increased NT. Methods: The study retrospectively analyzed 716 pregnant women with isolated increased NT in Group IiNT and 2960 pregnant women in the control group. The control group was divided into sub-Group A (1531 patients underwent invasive prenatal diagnosis for advanced maternal age (AMA)), sub-Group B (1331 for high-risk maternal serum screening (hMSS)), and sub-Group C (98 for both hMSS and AMA). All cases underwent karyotyping and chromosomal microarray analysis. Results: In Group IiNT and each sub-group, there were cases of RA (17, 28, 24, and 1) and clinically significant CNVs (22, 19, 39, and 5), respectively. There was no significant difference in RA incidence between Group IiNT and the control group/subgroups. Similarly, there was no statistical difference in clinically significant CNVs and CNVs <10 Mb between Group IiNT and sub-Group B/C or the control group. Only Group IiNT and sub-Group A showed a significant difference. Conclusion: Using NIPS with broader and deeper sequencing could theoretically potentially serve as a screening tool for identifying global chromosomal and submicroscopic abnormalities in fetuses with isolated increased NT. However, further research is required to determine the clinical application and to assess the efficacy of NIPS in detecting abnormalities. Traditional karyotyping and SNP array was performed on all 3676 pregnancies.
2023-04-30 | GSE230763 | GEO
Project description:We report 12 individuals from ten unrelated families with epilepsy, learning difficulties, intellectual disability, and neurobehavioral abnormalities, who segregated a microdeletion distally adjacent to the Williams-Beuren syndrome region. In six families, a recurrent ~ 1.1 Mb deletion likely resulted from nonallelic homologous recombination between flanking large complex low-copy repeats. Three smaller sized microdeletions (~ 180-500 kb) enabled us to narrow the critical region to one gene, HIP1, encoding Huntington interacting protein 1. genomic DNA from blood was used to analyse 12 samples with control sample using custom made NimbleGen 12x135K microarrays for chr7 region.
2010-08-28 | E-GEOD-23834 | biostudies-arrayexpress
Project description:Fetal DNA is present in the plasma of pregnant women. Massively parallel sequencing of maternal plasma DNA has been used to detect fetal trisomies 21, 18, 13 and selected sex chromosomal aneuploidies noninvasively. Case reports describing the detection of fetal microdeletions from maternal plasma using massively parallel sequencing have been reported. However, these previous reports were either polymorphism-dependent or used statistical analyses which were confined to one or a small number of selected parts of the genome. In this report, we reported a procedure for performing noninvasive prenatal karyotyping at 3 Mb resolution across the whole genome through the massively parallel sequencing of maternal plasma DNA. This method has been used to analyze the plasma obtained from 6 cases. In 5 cases, fetal microduplications or microdeletions have been detected successfully from maternal plasma. The two cases with fetal microduplications represented the first noninvasive prenatal detection of such changes from maternal plasma. In the remaining case, the plasma DNA sequencing result was consistent with the pregnant mother being a carrier of a microduplication. Simulation analyses were performed for determining the number of plasma DNA molecules that would need to be sequenced and aligned for enhancing the diagnostic resolution of noninvasive prenatal karyotyping to 2 Mb and 1 Mb. In conclusion, noninvasive prenatal molecular karyotyping from maternal plasma by massively parallel sequencing is feasible and would enhance the diagnostic spectrum of noninvasive prenatal testing.
| EGAS00001000439 | EGA
Project description:Maternal exposure to stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. The mechanisms through which the effects of maternal stress are transmitted to the fetus are unclear, however the placenta, as the interface between mother and fetus, is likely to play a key role. Using a rat model, we investigated a role for placental oxidative stress in conveying the effects of maternal social stress to the fetus and the potential for treatment using a nanoparticle-bound antioxidant to prevent adverse outcomes in the offspring. Maternal psychosocial stress increased circulating corticosterone in the mother, but not in the fetuses. Maternal stress also induced oxidative stress in the placenta, but not in the fetal brain. Blocking oxidative stress using an antioxidant prevented the prenatal stress-induced anxiety phenotype in the male offspring, and prevented sex-specific neurobiological changes, specifically a reduction in dendrite lengths in the hippocampus, as well as reductions in the number of parvalbumin-positive neurons and GABA receptor subunits in the hippocampus and basolateral amygdala of the male offspring. Importantly, many of these effects were mimicked in neuronal cultures by application of placental-conditioned medium or fetal plasma from stressed pregnancies, indicating molecules released from the placenta may mediate the effects of prenatal stress on the fetal brain. Indeed, both placenta-conditioned medium and fetal plasma contained differentially abundant microRNAs following maternal stress, and their predicted targets were enriched for genes relevant to nervous system development and psychiatric disorders. The results highlight placental oxidative stress as a key mediator in transmitting the maternal social stress effects on the offspring's brain and behaviour, and offer a potential intervention to prevent stress-induced fetal programming of affective disorders.
2020-12-01 | GSE130573 | GEO
Project description:We report 12 individuals from ten unrelated families with epilepsy, learning difficulties, intellectual disability, and neurobehavioral abnormalities, who segregated a microdeletion distally adjacent to the Williams-Beuren syndrome region. In six families, a recurrent ~ 1.1 Mb deletion likely resulted from nonallelic homologous recombination between flanking large complex low-copy repeats. Three smaller sized microdeletions (~ 180-500 kb) enabled us to narrow the critical region to one gene, HIP1, encoding Huntington interacting protein 1.
2010-08-28 | GSE23834 | GEO