Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

39 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

BBBomics - Human Blood Brain Barrier Transcriptomics Hub [RNA-seq]

ABSTRACT: Functional and structural dysfunction of the blood brain barrier (BBB) leads to severe alterations in brain physiology and is believed to trigger neurodegeneration. To investigate the molecular mechanisms driving the BBB dysfunction, very few human BBB cell culture models are available; of which, the human microvascular endothelial cell line (hCMEC/D3) is the most widely used. Thus far, array-based approaches or targeted seqeuncing based approaches have been employed to characterize the gene expression of the hCMEC/D3 model. However,The goal of this study is to perform deep transcriptomic sequencing of the BBB cell line and obtain features like gene expression, expressed single nucleotide variants, alternate splice forms, circular RNAs, long non-coding RNAs and micro RNAs. We have developed blood brain barriers transcriptomics landscape using RNA sequencing and micro RNA seqeuncing data obtained from replicates of hCMEC/D3 BBB cell line.

ORGANISM(S): Homo sapiens

SUBMITTER: Asha Nair

PROVIDER: E-GEOD-76528 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

BBBomics-Human Blood Brain Barrier Transcriptomics Hub.

Kalari Krishna R KR Thompson Kevin J KJ Nair Asha A AA Tang Xiaojia X Bockol Matthew A MA Jhawar Navya N Swaminathan Suresh K SK Lowe Val J VJ Kandimalla Karunya K KK

Frontiers in neuroscience 20160301

PMID: 26973449

Similar Datasets

BBBomics - Human Blood Brain Barrier Transcriptomics Hub [miRNA-seq]

Project description:Functional and structural dysfunction of the blood brain barrier (BBB) leads to severe alterations in brain physiology and is believed to trigger neurodegeneration. To investigate the molecular mechanisms driving the BBB dysfunction, very few human BBB cell culture models are available;of which, the human microvascular endothelial cell line (hCMEC/D3) is the most widely used. Thus far, array-based approaches or targeted seqeuncing based approaches have been employed to characterize the gene expression of the hCMEC/D3 model. However,The goal of this study is to perform deep transcriptomic sequencing of the BBB cell line and obtain features like gene expression, expressed single nucleotide variants, alternate splice forms, circular RNAs, long non-coding RNAs and micro RNAs. We have developed blood brain barriers transcriptomics landscape using RNA and micro RNA sequencing data obtained from replicates of hCMEC/D3 BBB cell line.

2016-03-17 | E-GEOD-76530 | biostudies-arrayexpress

BBBomics - Human Blood Brain Barrier Transcriptomics Hub [miRNA-seq]

2016-03-17 | GSE76530 | GEO

BBBomics - Human Blood Brain Barrier Transcriptomics Hub [RNA-seq]

Project description:Functional and structural dysfunction of the blood brain barrier (BBB) leads to severe alterations in brain physiology and is believed to trigger neurodegeneration. To investigate the molecular mechanisms driving the BBB dysfunction, very few human BBB cell culture models are available; of which, the human microvascular endothelial cell line (hCMEC/D3) is the most widely used. Thus far, array-based approaches or targeted seqeuncing based approaches have been employed to characterize the gene expression of the hCMEC/D3 model. However,The goal of this study is to perform deep transcriptomic sequencing of the BBB cell line and obtain features like gene expression, expressed single nucleotide variants, alternate splice forms, circular RNAs, long non-coding RNAs and micro RNAs.

2016-03-17 | GSE76528 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation (part 2)

Project description:Over-expression of miR-155 induces changes in the pattern of gene expression of hCMEC/D3 cells. hypothesis tested in the present study was that miR-155 constitute an important regulatory control of the brain endothelial response to inflammatory cytokines. To identify miR-155 target genes in brain endothelim that might be implicated in BBB dysfunction relevant to human disease, we then analysed changes in mRNA expression of hCMEC/D3 cells that overexpress miR-155 and results were contrasted to cells transfected with scrambled miR. To ectopically express miR-155 in hCMEC/D3 cells, 30 nM of pre-miR-155 and the siPORT Amine transfection agent (Applied Biosystems, Warrington, UK) were combined following the manufacturerM-bM-^@M-^Ys instructions.

2014-04-29 | E-GEOD-44693 | biostudies-arrayexpress

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation (part 1)

Project description:Here, we investigated the time-course changes in the pattern of microRNA (miRNA) expression of TNFα and IFNγ-stimulated and unstimulated hCMEC/D3 cells, an immortalized human cerebral microvascular endothelial cell line. In order to investigate pro-inflammatory cytokine-induced changes in miRNA levels in hCMEC/D3 cells, we challenged brain endothelial cells with TNFα and IFNγ (100 ng/ml) for 2 h, 6 h and 24 h and determined microRNA expression in cytokine-stimulated and unstimulated cells

2014-04-29 | E-GEOD-44692 | biostudies-arrayexpress

Human Blood Brain Barrier treated by Insulin

Project description:This study aims to map the dynamics of insulin-responsive pathways in polarized human cerebral microvascular endothelial cell (hCMEC/D3) monolayers, a widely used BBB cell culture model, to elucidate molecular mechanisms underlying BBB dysfunction in AD.

2022-02-05 | GSE195781 | GEO

Characterization of secretomes from brain microvascular endothelial cells after ischemia

Project description:The human immortalized brain endothelial cell line hCMEC/D3 is considered an in vitro model of the blood-brain-barrier. We aimed to characterize changes in the secretome of hCMEC/D3 subjected to oxygen and glucose deprivation (OGD) by SILAC, in order to identify new proteins involved in ischemia-triggered blood-brain-barrier disruption and test their potential as blood biomarkers for ischemic stroke diagnosis. After SILAC analysis, 19 proteins were found differentially secreted between OGD and normoxia/normoglycemia conditions (Fold Change>|1.4| and peptide count≥2). Protein folding and nucleic acid binding were the main molecular functions and epithelial adherens junctions and aldosterone signaling appeared as the main canonical pathways represented by OGD-secreted proteins. ANXA1, CLUS, IGFBP2, PRDX3, TIMP2 and COL1A2 were replicated by western blotting in 9 independent cell cultures. Five replicated proteins were analyzed in human serum samples of 38 ischemic stroke patients compared to 18 stroke-mimicking conditions and 18 healthy controls by ELISA. IGFBP2 showed increased blood levels when strokes were compared with stroke-mimicking patients (p<0.1). In conclusion, we characterized changes in the secretome of hCMEC/D3 after an ischemic insult and highlighted some candidates to become biomarkers for ischemic stroke diagnosis related to blood-brain-barrier disruption.

2016-01-21 | PXD002292 | Pride

Proteomic profiling of hCMEC/D3 cells exposed 3 days to laminar physiological shear stress

Project description:Endothelial cells (ECs) are constantly submitted in vivo to hemodynamical forces derived from the blood circulation, including shear stress (SS). EC are able to detect SS and consequently adapt their phenotype, thus affecting many endothelial functions. If a plethora of shear stress-regulated molecular networks have been described in peripheral EC, less is known about the molecular responses of microvascular brain ECs which constitute the blood-brain barrier (BBB). In this work, we investigated the response of human cerebral microvascular ECs to laminar physiological shear stress using the well characterized hCMEC/D3 cell line. Interestingly, we showed that hCMEC/D3 cells responded to shear stress by aligning perpendicularly to the flow direction, contrary to peripheral endothelial cells which aligned in the flow direction. Whole proteomic profiles were compared between hCMEC/D3 cells cultured either in static condition or under 5 or 10 dyn.cm-2 SS for three days. 3592 proteins were identified and expression levels were significantly affected for 3% of them upon both SS conditions. Pathway analyses were performed which revealed that most proteins overexpressed by SS refer to the antioxidant defense, probably mediated by activation of the NRF2 transcriptional factor. Regarding down-regulated proteins, most of them participate to the pro-inflammatory response, cell motility and proliferation. These findings confirm the induction of EC quiescence by laminar physiological SS and reveal a strong neuroprotective effect of SS on hCMEC/D3 cells, suggesting a similar effect on the BBB. Our results also showed that SS did not significantly increase expression levels nor did it affect the localization of junctional proteins or the functional activity of several ABC transporters (P-glycoprotein and MRPs). This work provides new insights on the response of microvascular brain EC to SS and on the importance of SS for optimizing in vitro BBB models.

2022-08-12 | PXD030493 | Pride

Cytokine-induced changes in the gene expression profile of human cerebral microvascular endothelial cell-line, hCMEC/D3

Project description:In the current study, we aimed to investigate the gene expression pattern in hCMEC/D3 cells using mRNA microarray analysis and to establish wheather hCMEC/D3 cells are a suitable in vitro human BBB model of neuroinflammation.

2013-09-16 | GSE45880 | GEO

Determination of effects of propionate on gene expression in human cerebromicrovascular endothelial cell line hCMEC/D3

Project description:The experiment was designed to look at the effect (on gene expression) of exposing human cerebromicrovascular endothelial cell line hCMEC/D3 to propionate (3 micromolar) for 24 h, to determine if circulating metabolites have the potential to affect integrity of the blood-brain barrier.

2018-03-05 | E-MTAB-5686 | 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