Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide transcriptome profiling Brain-Chip and Conventional Cell Culture System Using RNA-seq

ABSTRACT: The goal of this study was A) to compare the global RNA-sequencing (RNA-seq) profiles data of the neurovascular units constructed in i) conventional cell cultures (n=4), ii) Substantia Nigra Brain-Chips cultured under constant flow (n=4), and iii) human adult brain-derived substantia nigra (n=8) retrieved from the Genotype-Tissue Expression (GTEx) Portal, B) to identify differences in the transcriptome profiles in brain endothelial cells between the two conditions, αSyn fibrils and αSyn monomers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE168870 | GEO | 2021/09/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide transcriptome profiling Brain-Chip and Conventional Cell Culture System Using RNA-seq

Project description:The goal of this study was A) to compare the global RNA-sequencing (RNA-seq) profiles data of the neurovascular units constructed in i) conventional cell cultures (n=4), ii) Cortical Brain-Chips cultured under constant flow (n=4), and iii) human adult brain-derived contex (n=8) retrieved from the Genotype-Tissue Expression (GTEx) Portal.

2022-08-26 | GSE199787 | GEO

Uptake of alpha-synuclein preformed fibrils is suppressed by inflammation and induces an aberrant phenotype in human microglia

Project description:To detect the microglial mRNA signature whilst phagocytosing alphasynuclein preformed fibrils (αSyn PFFs) with or without inflammatory stimulus, we treated the healthy control microglia with IFNγ (20ng/ml) 28h and αSyn PFFs (0.5µM) 4h

2024-10-22 | GSE277636 | GEO

Spiked human substantia nigra proteome data set for use as a spectral library for protein modelling and protein mapping

Project description:This article describes a mass spectrometry data set generated from human substantia nigra tissue that was spiked with iRT peptides. The data set can be used as a spectral library for analysis of the human brain, especially human substantia nigra, for example, in the context of Parkinson’s disease. Obtaining a sufficient amount of high-quality substantia nigra tissue is the key limiting factor for establishing a brain region-specific spectral library. Hence, combining existing spectral libraries for data-independent acquisition analysis (DIA) can overcome this major limitation. Moreover, these data can be used to map brain region-specific proteins and to model brain region-specific pathways. Both can improve our understanding of the functioning of the brain in greater depth. In addition, these data can also be used to determine the optimal settings for measuring proteins and peptides of interest. To create the substantia nigra-specific spectral library, the tissue was first homogenized and then fractionated via different types of SDS gel electrophoresis, resulting in 18 fractions. These fractions were analysed in triplicate by nanoHPLC-ESI-MS/MS, resulting in 54 data files.

2019-08-15 | PXD011076 | Pride

Transcriptome-wide changes in the Substantia Nigra following Deep Brain Stimulation in the Subthalamic Nuecleus of a PD rat model.

Project description:In this study we identify the gene espression changes that occur in the substantia nigra in a Parkinson's Disease (PD) rat model with and without deep brain stimulation (DBS). A rat model of PD was created as previously described by stereotacticaly injecting an AAV-expressing the human A53T_mutated form of a-Synuclein into the Substantia Nigra of adult rats, while control rats were injected with empty vector (EV). These mice exhibit neurodegeneration in the Substantia Nigra and Parkinson-like behaviour phenotypes. Sixteen weeks after the injection, RNA was isolated from the Substantia Nigra and Striatum. Single-end 75nt high throughput sequencing were performed on libraries prepared from the RNA. We identified over 200 genes that were differentially expressed between control and Parkinson's ratswith a log2 fold-change > |0.6|. These genes were enriched for terms related to immune activation. The genes associated with these GO terms tended to be up-regulated in the Parkinson's rats suggesting that brain-localized immune cells are more activated in Parkinson's disease. Interestingly in the rats treated with DBS, these immune-related genes were comparable to control animals.

2024-12-09 | GSE263579 | GEO

RNA-SEQ profiling of dopaminergic neurons from the substantia nigra pars compacta and ventral tegmental area regions of the mouse mid-brain

Project description:RNA-SEQ profiling of dopaminergic neurons from the substantia nigra pars compacta and ventral tegmental area regions of the mouse mid-brain

2015-07-27 | GSE64452 | GEO

Next generation sequencing reveals upregulation of the lncRNA LINC-PINT in the substantia nigra of human Parkinson's disease patients compared to control donors

Project description:Parkinson's disease (PD) is the second most common neurodegenerative disease, involving the selecive death of dopaminergic neurons in the substantia nigra pars compacta brain region. Here, we performed next generation sequencing on RNA extracted from human substantia nigra tissue. The samples, acquired from the Netherland's Brain Bank, were taken post-mortem from PD and non-PD control donors. Analysis of the data revealed an upregulation of lncRNA LINC-PINT in PD substantia nigra. LINC-PINT interracts with the Polycomb Repressive Complex 2 (PRC2), inhibiting the tracription of multiple targets. Correspondingly, analysis of the data revealed that targets of PRC2 displayed larger disease-associated differences as compared to other genes, as well as enrichment for downregulation, suggesting that the differential expression of LINC-PINT in PD effects LINC-PINT/PRC2 interaction as well.

2020-04-14 | GSE114517 | GEO

Control (healthy) iPSC-derived astrocytes treated with: Media (control) or aSYN F110 10uM

Project description:The overall goal was to identify changes in gene expression following treatment with aSYN F110 compared to control (untreated). Alpha-synuclein (αSYN) protein has been observed in reactive astrocytes in PD patients’ brains, raising the question of how αSYN, neuroinflammation, and astrocytes interact in PD pathogenesis. Here, we examined the cellular changes triggered by tumor necrosis factor alpha (TNFα) and different αSYN species in astrocytes derived from induced pluripotent stem cells. Human astrocytes treated with TNFα displayed a strong reactive pro-inflammatory phenotype with upregulation of pro-inflammatory gene networks, activation of the NF-kB pathway, and release of pro-inflammatory cytokines, whereas those treated with high molecular weight αSYN fibrils acquired a reactive antigen (cross-)presenting phenotype with upregulation of MHC genes and increased HLA-DR/DQ/DP and HLA-F molecules at the cell surface. Surprisingly, cell surface location of MHC proteins was abrogated by larger F110 fibrils polymorph, despite the upregulation of MHC genes. A proteomics investigation further confirmed a direct interaction between astrocytic MHC proteins and αSYN fibril peptides. Interestingly, TNFα and αSYN fibrils competed to drive the astrocyte immune reactive response. The astrocyte immune responses were accompanied by an impaired ATP-generating mitochondrial respiration, which was exacerbated in PD astrocytes containing a PARK2-variant. Our data provide evidence for astrocytic involvement in PD pathogenesis and reveal their complex immune reactive responses to exogenous stressors.

2021-02-16 | GSE166769 | GEO

Substantia nigra (SN) and basal ganglia (BG) gene expression in neurodegenertion with brain iron accumulation (NBIA) cases vs normal controls

Project description:Differential gene expression is assessed in substantia nigra and basal ganglia of neurodegenertion with brain iron accumulation cases (BIA) compared to matched normal controls (c).

2017-02-09 | GSE70430 | GEO

Control (healthy) iPSC-derived astrocytes treated with: Media (control), TNFa 100ug/ml, Monomeric aSYN 10uM, or Fibril aSYN 10uM

Project description:The overall goal was to identify changes in gene expression following treatment with TNFa, monomeric, or fibril aSYN compared to control (untreated). Alpha-synuclein (αSYN) protein has been observed in reactive astrocytes in PD patients’ brains, raising the question of how αSYN, neuroinflammation, and astrocytes interact in PD pathogenesis. Here, we examined the cellular changes triggered by tumor necrosis factor alpha (TNFα) and different αSYN species in astrocytes derived from induced pluripotent stem cells. Human astrocytes treated with TNFα displayed a strong reactive pro-inflammatory phenotype with upregulation of pro-inflammatory gene networks, activation of the NF-kB pathway, and release of pro-inflammatory cytokines, whereas those treated with high molecular weight αSYN fibrils acquired a reactive antigen (cross-)presenting phenotype with upregulation of MHC genes and increased HLA-DR/DQ/DP and HLA-F molecules at the cell surface. Surprisingly, cell surface location of MHC proteins was abrogated by larger F110 fibrils polymorph, despite the upregulation of MHC genes. A proteomics investigation further confirmed a direct interaction between astrocytic MHC proteins and αSYN fibril peptides. Interestingly, TNFα and αSYN fibrils competed to drive the astrocyte immune reactive response. The astrocyte immune responses were accompanied by an impaired ATP-generating mitochondrial respiration, which was exacerbated in PD astrocytes containing a PARK2-variant. Our data provide evidence for astrocytic involvement in PD pathogenesis and reveal their complex immune reactive responses to exogenous stressors.

2021-02-16 | GSE166768 | GEO

Human α-synuclein overexpression upregulates SKOR1 in a rat model of simulated nigrostriatal aging

Project description:Parkinson’s disease is characterised by progressive loss of dopaminergic (DA) neurons from the substantia nigra (SN) and intraneuronal accumulation of α-synuclein (αSyn) protein. Age is the biggest risk factor for Parkinson’s and has been suggested to create a vulnerable pre-parkinsonian state, but the drivers of this association are unclear. It is known that aging leads to increased αSyn expression in DA neurons and it is possible that this may alter molecular processes that are central to maintaining nigrostriatal integrity. To investigate this, adult female Sprague-Dawley rats received unilateral intranigral injection of adeno-associated viral (AAV) vector carrying wild-type human αSyn (AAV-αSyn) or control vector (AAV-Null). AAV-αSyn induced no detrimental effects on motor behaviour, but there was expression of human wild-type αSyn throughout the midbrain and ipsilateral striatum at 20 weeks post-surgery. Microarray analysis revealed that the gene most-upregulated in the ipsilateral SN of the AAV-αSyn group was the SKI Family Transcriptional Corepressor 1 (SKOR1). Bioenergetic state analysis of mitochondrial function found that SKOR1 overexpression reduced the maximum rate of cellular respiration. Furthermore, SKOR1 impaired neurite growth to the same extent as α-synuclein, and inhibited BMP-SMAD-dependent transcription, a pathway that promotes DA neuron survival and growth. Given the normal influence of ageing on DA neuron loss in human SN, the extent to which αSyn upregulates SKOR1 may influence whether an individual undergoes normal nigrostriatal ageing or reaches a threshold for prodromal PD. This provides new insight into mechanisms through which age-related changes may influence molecular mechanisms controlling neuronal integrity across the lifespan.

2024-08-08 | GSE252918 | GEO

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