RNASeq analysis of offspring ileum tissue following Prenatal stress
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ABSTRACT:
PROVIDER: PRJNA637902 | ENA |
REPOSITORIES: ENA
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Project description:Following a prenatal stress model, we collected RNA from ileum of offspring at 2 weeks of age. We sequenced the RNA to identify genes that are differentially expressed compared to offspring from unstressed controls. We identified DEGs and a number of biological and signaling pathways in the offsping in response to gesstational stress. We discuss the implications of these stress-induced genes on the development of inflammatory diseases in the gut of the offsping.
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Project description:Prenatal stress (PS) could cause depression of offprsing. Here, relative quantitative phosphoproteomics of hippocampus of PS-S and CON offspring rats were performed using LC-MS/MS to confirm known pathways and identify new areas of depression. A total of 6,790 phosphopeptides, 9,817 phosphorylation sites and 2978 phosphoproteins were detected. Among the 2978 phosphoproteins, 1760 (59.09%) with more than two phosphorylated sites, ENSRNOP00000023460 protein has more than 117 phosphorylated sites, and the average distribution of modification sites per 100 amino acids was 2.97. There were 197 different phophpeptides, including 140 increased phosphopeptides and 57 decreased phosphopeptides in PS-S offspring rats when compared to the CON offspring rats. These differential phosphopeptides corresponded to 100 upregulated and 44 downregulated phosphoproteins respectively. GO enrichment analysis these different phosphoproteins in the first five enrichments of CC category, MF category and BP category were involved in a total of 35 different phosphoproteins and these phosphoproteins were mainly related to myelin, microtubule and synapse associated proteins. The first five enrichment of KEGG pathways were found to be involved in many essential biological pathways, and the first five pathways included amphetamine addiction, insulin secretion, cushing syndrome and circadian entrainment signaling pathway. And these first five pathways were related to nine proteins including Adcy9, Apc, Cacna1c, Camk2a, Camk2b, Camk2g, Ctnnd2, Grin2a, Stx1a. Further research is needed to understand the precise role of these pathways in the depressive-like behavior of offspring rats caused by PS.
2021-12-30 | PXD019117 | Pride
Project description:Maternal exposure to social stress during pregnancy is associated with an increased risk of psychiatric disorders in the offspring in later life. How the effects of maternal social stress are transmitted to the developing foetus is unclear. Using a rat model of maternal social stress during pregnancy, we explored the mechanisms by which maternal stress is conveyed to the foetus and the potential for targeted treatment to prevent disease in the offspring. Maternal stress induced oxidative stress in the placenta, but not in the foetal brain, which was prevented by a single administration of nanoparticle-bound antioxidant prior to the stress exposure. Moreover, this antioxidant treatment prevented prenatal stress-induced anxiety-like behaviour in juvenile male offspring, along with neurological and gene expression changes in the offspring brain. In vitro, placental conditioned medium or foetal plasma from stressed pregnancies caused changes to cultured cortical neurons, similar to those observed in the brains of juvenile offspring exposed to prenatal stress, and were found to contain altered levels of extracellular microRNAs but not corticosterone. The present study highlights the crucial role of the placenta, and molecules secreted from the placenta, in foetal brain development and provides evidence of the potential for treatment that can prevent maternal stress-induced foetal programming of neurological disease.
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Project description:Prenatal stress is one of the risk factors for the development of mental disorders in offspring, but its underlying mechanism remains elusive. To perform epigenomic profiling of prenatal stress effects on fetal brains, ATAC-seq and RNA-seq were used to explore the changes of chromatin accessibility and gene expression on embryonic brains at E15.5 of offspring from pregnant mice, which were exposed to chronic mild unpredictable stress between E5.5 to E14.5.
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Project description:DNA methylation profiling of CD34 positive cells derived from cord blood at birth following prenatal stress The groups consist of 8 individuals with low levels of prenatal stress (control) and 10 individuals with high levels of prenatal stress (stress)
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Project description:Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental disorder that significantly jeopardizes the physical and mental well-being of children. Autism spectrum disorder results from a combination of environmental and genetic factors. Hyperandrogenic exposure during pregnancy increases their risk of developing autism. Nevertheless, the prenatal exposure to androgens affects offspring neurodevelopment and the underlying mechanisms have not been fully elucidated. In the present study, administration of excessive dihydrotestosterone (DHT) to pregnant mice was found to impair neuronal development and dendritic spine formation in offspring, inducing autism-like behaviors. Furthermore, through mRNA transcriptome sequencing technology, the key molecule Nr4a2 was identified during this process of change. Overexpression of Nr4a2 and treatment with amodiaquine (AQ) significantly improved the abnormal phenotypes in offspring caused by prenatal exposure to androgens. Overall, Nr4a2 emerges as a crucial molecule involved in the impairment of offspring neurodevelopment due to prenatal androgen exposure, which provides a new perspective for the in-depth study of the influencing factors and underlying mechanisms.
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Project description:DNA methylation profiling of CD34 positive cells derived from cord blood at birth following prenatal stress
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Project description:Prenatal exposure to infectious or inflammatory insults can increase the risk of neuropsychiatric disorders with neurodevelopmental components, including schizophrenia and autism. The molecular processes underlying this pathological association are only partially understood. Here, we implemented an unbiased genome-wide transcriptional profiling of the prefrontal cortex of mice exposed to prenatal infection on GD17 compared to control subjects in order to elucidate the long term molecular signature of late prenatal infection. We used microarray analysis to investigate the long lasting gene expression changes in a well-established mouse model that is based on maternal treatment with the viral mimic poly(I:C) during pregnancy C57BL/6 mice were treated with the synthetic viral mimetic poly(I:C) (5 mg/kg, i.v.) or control (saline, i.v.) solution on gestation day 17. Offspring were subjected to cognitive and behavioral testing in adulthood, and then whole genome gene expression analysis with Affymetrix Microarray and subsequent q-PCR validation were performed on the prefrontal Cortex.
2016-03-01 | E-GEOD-77972 | biostudies-arrayexpress
Project description:Prenatal exposure to infectious or inflammatory insults can increase the risk of neuropsychiatric disorders with neurodevelopmental components, including schizophrenia and autism. The molecular processes underlying this pathological association are only partially understood. Here, we implemented an unbiased genome-wide transcriptional profiling of the nucleus accumbens of mice exposed to prenatal infection on GD17 compared to control subjects in order to elucidate the long term molecular signature of late prenatal infection. We used microarray analysis to investigate the long lasting gene expression changes in a well-established mouse model that is based on maternal treatment with the viral mimic poly(I:C) during pregnancy C57BL/6 mice were treated with the synthetic viral mimetic poly(I:C) (5 mg/kg, i.v.) or control (saline, i.v.) solution on gestation day 17. Offspring were subjected to cognitive and behavioral testing in adulthood, and then whole genome gene expression analysis with Affymetrix Microarray and subsequent q-PCR validation were performed on the nucleus accumbens.
2016-03-01 | E-GEOD-77971 | biostudies-arrayexpress
Project description:Purpose: Gestational exposure to environmental toxins and socioeconomic stressors are epidemiologically linked to neurodevelopmental disorders with strong male-bias, such as autism. We modeled these prenatal risk factors in mice, by co-exposing pregnant dams to an environmental pollutant and limited-resource stress, which robustly activated the maternal immune system. Only male offspring displayed long-lasting behavioral abnormalities and alterations in the activity of brain networks encoding social interactions. Cellularly, prenatal stressors diminished microglial function within the anterior cingulate cortex, a central node of the social coding network, in males during early postnatal development. Genetic ablation of microglia during the same critical period mimicked the impact of prenatal stressors on a male-specific behavior, indicating that environmental stressors alter neural circuit formation in males via impairing microglia function during development.
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