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 sequencing and micro RNA seqeuncing data obtained from replicates of hCMEC/D3 BBB cell line.
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.
Project description:The aim of this study is to understand how NMV can affect the vascular integrity of the blood-brain barrier using a cell line- hCMEC/D3. Recent studies have reported that NMV can affect other endothelial barriers in the body contributing to inflammation and pathogenesis of diseases such as atherosclerosis. The transcriptomic profile of NMV-treated hCMEC/D3 cells was compared to that of cells without treatment to understand whether functional groupings and pathways are differentially expressed, which can contribute to changes in blood-brain barrier.
Project description:To study the impact of inflammation on the blood-brarrier permeability we choose to expose hCMEC/D3 cells, a blood-brain barrier cell line, to interleukin-6 as an inflammatory marker.
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.
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.
Project description:The experiment was designed to look at the effect (on gene expression) of exposing human cerebromicrovascular endothelial cell line hCMEC/D3 to trimethylamine (0.4 micromolar) or trimethylamine N-oxide (40 micromolar) for 24 h, to determine if circulating metabolites have the potential to affect integrity of the blood-brain barrier.
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.
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.
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