Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Modeling maternal cholesterol exposure reveals a reduction of neural progenitor proliferation using human cerebral organoids

ABSTRACT: Modeling maternal cholesterol exposure reveals a reduction of neural progenitor proliferation using human cerebral organoids

PROVIDER: PRJNA851425 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19768962_1.fastq.gz	Fastqsanger.gz
	SRR19768962_2.fastq.gz	Fastqsanger.gz
	SRR19768963_1.fastq.gz	Fastqsanger.gz
	SRR19768963_2.fastq.gz	Fastqsanger.gz
	SRR19768964_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Modeling maternal cholesterol exposure reveals a reduction of neural progenitor proliferation using human cerebral organoids

Project description:Maternal obesity raises the risk of high-cholesterol exposure for their offspring. Studies in cohorts and animal models report that maternal obesity could increase the risk of neurodevelopmental disorders (NDDs) in offspring including intellectual disabilities and autism spectrum disorders (ASD). However, whether exposure to high cholesterol is responsible for brain developmental defects, as well as its underlying mechanism, is still unclear. Here, we constructed a cholesterol exposure model utilizing hiPSC-derived cerebral organoids by exogenously adding cholesterol into the culture system. We preformed scRNA sequence analysis to explore the gene expression changes in brain organoids under additional cholesterol exposure.

2022-12-31 | GSE206587 | GEO

Human Tau Mutations in Cerebral Organoids Induce a Progressive Dyshomeostasis of Cholesterol

Project description:Mutations in the MAPT gene that encodes tau lead to frontotemporal dementia (FTD) with pathology evident in both cerebral neurons and glia. Human cerebral organoids (hCOs) from individuals harboring pathogenic tau mutations can reveal the earliest downstream effects on molecular pathways within a developmental context generating interacting neurons and glia. We found that in hCOs carrying the V337M and R406W tau mutations, the cholesterol biosynthesis pathway in astrocytes was the top upregulated gene set compared to isogenic controls by scRNAseq. The 15 upregulated genes included HMGCR, ACAT2, STARD4, LDLR, and SREBF2. This result was confirmed in a homozygous R406W mutant cell line, by immunostaining and sterol measurements. Cholesterol abundance in the brain is tightly regulated by efflux and cholesterol biosynthetic enzyme levels in astrocytes, and dysregulation can cause aberrant phosphorylation of tau. Our findings suggest that cholesterol dyshomeostasis is an early event in the etiology of neurodegeneration caused by tau mutations.

2022-07-21 | GSE208418 | GEO

The endogenous protein-protein interaction network of the NPC Cholesterol Transporter 1 in the cerebral cortex

Project description:The endogenous protein-protein interaction network of the NPC Cholesterol Transporter 1 in the cerebral cortex

2023-11-12 | MSV000093378 | MassIVE

Hepatic inactivation of murine Surf4 results in marked reduction in plasma cholesterol

Project description:Hepatic inactivation of murine Surf4 results in marked reduction in plasma cholesterol

| PRJNA885114 | ENA

Cerebral organoids proteomics - Human Cerebral Organoids and Fetal Brain Tissue Share Proteomic Similarities

Project description:Pluripotent stem cells (PSC) can differentiate inot any cell type of an organism. Their remarkable capability of self-organization enables the formation of three-dimensional structures that resembles miniature organs, including cerebral organoids. These organoids can recreate early steps of the human cerebral cortex development, and show great potential for modeling human diseases, particularly for those with a developmental component. This data evidences stem cell-derived cerebral organoids as a key model to study brain development and neurodevelopmental, neurodegenerative and neuropsychiatric diseases.

2019-11-15 | PXD011605 | Pride

Human Tau Mutations in Cerebral Organoids Induce a Progressive Dyshomeostasis of Cholesterol

Project description:Human Tau Mutations in Cerebral Organoids Induce a Progressive Dyshomeostasis of Cholesterol

| PRJNA859858 | ENA

Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism

Project description:The brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis. Here we demonstrate that in insulin-deficient diabetic mice, there is a reduction in expression of the major transcriptional regulator of cholesterol metabolism, SREBP-2, and its downstream genes in the hypothalamus and other areas of the brain, leading to a reduction in brain cholesterol synthesis and synaptosomal cholesterol content. These changes are due, at least in part, to direct effects of insulin to regulate these genes in neurons and glial cells and can be corrected by intracerebroventricular injections of insulin. Knockdown of SREBP-2 in cultured neurons causes a decrease in markers of synapse formation and reduction of SREBP-2 in the hypothalamus of mice using shRNA results in increased feeding and weight gain. Thus, insulin and diabetes can alter brain cholesterol metabolism, and this may play an important role in the neurologic and metabolic dysfunction observed in diabetes and other disease states. Hypothalamus was compared between streptozotocin (STZ)-induced diabetic, ob/ob, and control mice, with 5-6 replicates per goup.

2014-10-03 | E-GEOD-62013 | biostudies-arrayexpress

Diabetes and Insulin in Regulation of Brain Cholesterol Metabolism

2014-10-03 | GSE62013 | GEO

Modeling Genetic Epileptic Encephalopathies using Brain Organoids

Project description:We generated cerebral organoids from genetically engineered human embryonic stem cells (hESCs), modeling the devastating WOREE syndrome (DEE28), as a prototype for genetic epileptic encephalopathies (EEs). Transcriptome analysis of mutated organoids compared to the WT revealed molecular changes related to both early infantile EEs and specifically to WOREE syndrome.

2021-07-01 | GSE156243 | GEO

Expression data from control and Smith-Lemli-Opitz syndrome patient-derived iPS cells - comparison of cholesterol deficient and cholesterol rich culture

Project description:7-dehydrocholesterol reductase catalyzes the reduction of 7-dehydrocholesterol to cholesterol. In Smith-Lemli-Opitz syndrome, mutations in DHCR7 prevents this conversion. We have found iPS cells derived from SLOS patients exhibit accelerated differentiation under cholesterol poor conditions. In this dataset, we include expression data obtained from comparision of a control iPS cell line (BJ) and a SLOS iPS cell line (A2). Cell line gene expression was compared in cholesterol rich conditions where the SLOS phenotype is suppressed. Cholesterol deficient culture of control and SLOS iPS cells demonstrated enhanced differentiation of SLOS cells over 7 days. These data are used to obtain 308 genes that are differentially expressed upon cholesterol deficient culture. time-course expression data obtained from control and SLOS patient iPS cells after transfer from cholesterol rich to cholesterol deficient culture. 48 total RNA samples were isolated and hybridized on Affymetrix arrays. We generated the following pairwise comparisons using Partek: BJ 0hr vs A2 0hr; BJ 2Day vs A2 2Day; BJ 3Day vs A2 3Day; BJ 4Day vs A2 4Day; BJ 5Day vs A2 5Day; BJ 7Day vs A2 7Day. Genes with an FDR≤10% and a fold-change ≥3 were identified as significantly different. We also performed pairwise comparison of BJ and A2 samples within each cell line between subsequent isolations (i.e. BJ 0hr vs BJ 2Day; A2 3Day vs A2 4Day; etc.)

2015-09-18 | E-GEOD-61203 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data