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Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Bisulfite-Seq)

ABSTRACT: Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Bisulfite-Seq)

PROVIDER: PRJNA977657 | ENA |

REPOSITORIES: ENA

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Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus

Project description:Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus

| PRJNA977655 | ENA

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (RNA-Seq)

Project description:Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (RNA-Seq)

| PRJNA977660 | ENA

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Targeted EM-Seq)

Project description:Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Targeted EM-Seq)

| PRJNA977658 | ENA

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Bisulfite-Seq)

Project description:To investigate the effects of maternal adiposity and leptin on fetal brain development, fetal hippocampal brain tissue and DNA was collected at 0.9 term for targeted EM-Seq analysis

2024-05-15 | GSE233720 | GEO

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (RNA-Seq)

Project description:To investigate the effects of maternal adiposity and leptin on fetal brain development, fetal hippocampal brain tissue was collected at 0.9 term for bulk RNA Seq analysis

2024-05-15 | GSE233724 | GEO

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus (Targeted EM-Seq)

2024-05-15 | GSE233721 | GEO

Maternal Adiposity Alters Transcriptomic and Epigenomic Neurodevelopmental Landscapes in the Fetal Hippocampus

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-15 | GSE233729 | GEO

CIDR_Visceral Adiposity

Project description:CIDR_Visceral Adiposity

| PRJNA75481 | ENA

Early or Late Gestational Exposure to Maternal Immune Activation Alters Neurodevelopmental Trajectories in Mice: An Integrated Neuroimaging, Behavioral, and Transcriptional Study

Project description:Background: Exposure to maternal immune activation (MIA) in utero is a risk factor for neurodevelopmental disorders later in life. The impact of the gestational timing of MIA exposure on downstream development remains unclear. Methods: We characterized neurodevelopmental trajectories of mice exposed to the viral mimetic poly I:C (polyinosinic:polycytidylic acid) either on gestational day 9 (early) or on day 17 (late) using longitudinal structural magnetic resonance imaging from weaning to adulthood. Using multivariate methods, we related neuroimaging and behavioral variables for the time of greatest alteration (adolescence/early adulthood) and identified regions for further investigation using RNA sequencing. Results: Early MIA exposure was associated with accelerated brain volume increases in adolescence/early adulthood that normalized in later adulthood in the striatum, hippocampus, and cingulate cortex. Similarly, alterations in anxiety-like, stereotypic, and sensorimotor gating behaviors observed in adolescence normalized in adulthood. MIA exposure in late gestation had less impact on anatomical and behavioral profiles. Multivariate maps associated anxiety-like, social, and sensorimotor gating deficits with volume of the dorsal and ventral hippocampus and anterior cingulate cortex, among others. The most transcriptional changes were observed in the dorsal hippocampus, with genes enriched for fibroblast growth factor regulation, autistic behaviors, inflammatory pathways, and microRNA regulation. Conclusions: Leveraging an integrated hypothesis- and data-driven approach linking brain-behavior alterations to the transcriptome, we found that MIA timing differentially affects offspring development. Exposure in late gestation leads to subthreshold deficits, whereas exposure in early gestation perturbs brain development mechanisms implicated in neurodevelopmental disorders.

2021-06-18 | GSE178403 | GEO

Social isolation-induced transcriptomic changes in mouse hippocampus impact the synapse and show convergence with human genetic risk for neurodevelopmental phenotypes

Project description:Early life stress (ELS) can impact brain development and is a risk factor for neurodevelopmental disorders such as schizophrenia. Post-weaning social isolation (SI) is used to model ELS in animals, using isolation stress to disrupt a normal developmental trajectory. We aimed to investigate how SI affects the expression of genes in mouse hippocampus and to investigate how these changes related to the genetic basis of neurodevelopmental phenotypes. BL/6J mice were exposed to post-weaning SI (PD21-25) or treated as group-housed controls (n = 7-8 per group). RNA sequencing was performed on tissue samples from the hippocampus of adult male and female mice. Four hundred and 1,215 differentially-expressed genes (DEGs) at a false discovery rate of < 0.05 were detected between SI and control samples for males and females respectively. DEGS for both males and females were significantly overrepresented in gene ontologies related to synaptic structure and function, especially the post-synapse. DEGs were enriched for common variant (SNP) heritability in humans that contributes to risk of neuropsychiatric disorders (schizophrenia, bipolar disorder) and to cognitive function. DEGs were also enriched for genes harbouring rare de novo variants that contribute to autism spectrum disorder and other developmental disorders. Finally, cell type analysis revealed populations of hippocampal astrocytes that were enriched for DEGs, indicating effects in these cell types as well as neurons. Overall, these data suggest a convergence between genes dysregulated by the SI stressor in the mouse and genes associated with neurodevelopmental disorders and cognitive phenotypes in humans.

2023-11-02 | GSE246551 | GEO

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