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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44693 | GEO | 2014/04/29

SECONDARY ACCESSION(S): PRJNA191031

REPOSITORIES: GEO

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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

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

2014-04-29 | GSE44692 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation

Project description:MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation

| PRJNA191023 | ENA

Neutrophil-derived microvesicle induced dysfunction of the blood-brain barrier in vitro

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.

2019-12-05 | GSE137111 | GEO

MiR-155 promotes blood-brain barrier dysfunction in neuroinflammation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-04-29 | E-GEOD-44694 | biostudies-arrayexpress

miR-155 plays selective cell-intrinsic roles in brain infiltrating immune cell populations during neuroinflammation

Project description:The pro-inflammatory microRNA-155 (miR-155) is highly expressed in the serum and CNS lesions of patients with multiple sclerosis (MS). The whole-body deletion of miR-155 in mice confers resistance to a mouse model of MS, EAE, by reducing the encephalogenic potential of CNS-infiltrating Th17 T cells. However, cell intrinsic roles for miR-155 during EAE have not been formally determined. Here we utilize single-cell RNA sequencing and cell-specific conditional miR-155 knockouts to determine the importance of miR-155 expression in distinct immune cell populations. Time course single-cell sequencing revealed reductions in T cells, macrophages, and dendritic cells in whole-body miR-155 knockout mice compared with wild-type controls at day 21. Deletion of miR-155 in T cells, driven by CD4 cre, reduced disease severity similar to whole-body miR-155 knockouts. CD11c cre-driven deletion of miR-155 in dendritic cells also significantly reduced EAE disease score, with both T cell and dendritic cell-specific knockouts showing a reduction in Th17 T cell infiltration into the CNS. Although miR-155 is highly expressed in infiltrating macrophages during EAE, deletion of miR-155 using LysM cre did not affect disease severity. Taken together, these data show that while miR-155 is highly expressed in most infiltrating immune cells, miR-155 has distinct roles and requirements depending on the cell type. This provides insights into which functionally relevant cell types should be targeted by the next generation of miRNA therapeutics.

2023-06-13 | GSE206056 | 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. 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.

2016-03-17 | E-GEOD-76528 | biostudies-arrayexpress

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

Hypoxia inducible microRNA-155 negatively regulates epithelial barrier in Eosinophilic Esophagitis by suppressing Tight Junction Claudin-7

Project description:MicroRNA (miRNA)-mediated mRNA regulation directs many homeostatic and pathological processes, but how miRNAs coordinate aberrant esophageal inflammation during eosinophilic esophagitis (EoE) is poorly understood. Here, we report a deregulatory axis where microRNA-155 (miR-155) regulates epithelial barrier dysfunction by selectively constraining tight junction CLDN7 (claudin-7). MiR-155 is elevated in the esophageal epithelium of biopsies from patients with active EoE and in cell culture models. miR-155 localisation using in situ hybridisation (ISH) in patient biopsies, and intra-epithelial compartmentalisation of miR-155 shows expression predominantly within the basal epithelia. Epithelial miR-155 activity was evident through diminished target gene expression in 3D organotypic cultures, particularly in relatively undifferentiated basal cell states. Mechanistically, generation of a novel cell line with enhanced epithelial miR-155 stable overexpression induced a functionally deficient epithelial barrier in 3D air-liquid interface epithelial cultures measured by transepithelial electrical resistance (TEER). Histological assessment of 3D esophageal organoid cultures overexpressing miR-155 showed notable dilated intra-epithelial spaces. Unbiased RNA-sequencing analysis and immunofluorescence determined a defect in epithelial barrier tight junctions and revealed a selective reduction in the expression of critical esophageal tight junction molecule, claudin-7. Together, our data reveal a previously unappreciated role for miR-155 in mediating epithelial barrier dysfunction in esophageal inflammation.

2023-12-12 | GSE244629 | GEO

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