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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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			Action	DRS
	SRR24765445_1.fastq.gz	Fastqsanger.gz
	SRR24765445_2.fastq.gz	Fastqsanger.gz
	SRR24765446_1.fastq.gz	Fastqsanger.gz
	SRR24765446_2.fastq.gz	Fastqsanger.gz
	SRR24765447_1.fastq.gz	Fastqsanger.gz

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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

Adiposity alters protective mechanisms of progesterone through dysregulation of endometrial metallothionein expression

Project description:In this study, we sought to understand the effects of excess adipose on the benign endometrium. We used a physiologic in vitro coculture system consisting of multicellular organoids of the benign human endometrium and adipose spheroids in the presence of estradiol, progesterone, and testosterone to mimic the menstrual cycle. Gene expression analysis of endometrial organoids under high adiposity conditions revealed downregulation of genes normally expressed in secretory endometrium, suggestive of an altered progesterone response. Genes associated with ion homeostasis and detoxification of reactive oxygen species were also downregulated, including the metallothionein (MT) family of genes. We demonstrated that MT gene expression in endometrial organoids was regulated by progesterone specifically in the epithelial cells, and that progesterone receptor is recruited to the promoters of MT genes in endometrial epithelial cells. We illustrated the impact of MT dysregulation by silencing MT genes in endometrial epithelial cells, resulting in increased DNA damage. Our results reveal that exposing the endometrium to high adiposity can compromise the protective effects of progesterone, dysregulate MT genes in the endometrial epithelium, and leave the endometrium vulnerable to ROS-induced DNA damage.

2024-04-19 | GSE240926 | GEO

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