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: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
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.
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.
Project description:Electronic cigarette (EC) use has grown substantially since entry into the US market, particularly among adolescents and combustible tobacco users. Despite growing popularity and claims of harm reduction, the health effects of these products outside the lung is poorly understood. Several constituents of cigarette smoke (CS) with known neurovascular and inflammatory effects are present in EC liquids or formed during the generation of vapor. The present study characterizes the impact of EC exposure on neuroinflammation and blood-brain barrier (BBB) function, and provides comparison of outcomes with reference cigarette exposure normalized to comparable levels of nicotine delivery. Additionally, the contribution of nicotine to observed effects is elucidated through comparison with EC liquids which are verified to be nicotine-free. C57BL/6 mice are exposed to 2 hrs of daily EC vapor or CS, beginning at 8 wks of age. Changes in BBB gene expression are first characterized by whole exome sequencing of isolated brain microvessels following chronic (2 month) EC exposure.