Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA116149 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We used microarrays to determine if miRNA expression in human airway smooth muscle cells is altered by a pro-inflammatory stimulus. A majority of the miRNAs on the array exhibited very low signal intensity. In ASM cells exposed to IL-1β, TNFα, and IFNγ, none of the miRNA expressed were significantly up-regulated with cytokine treatment. We did observe 11 miRNA down-regulated > 2-fold in both cultures with cytokine treatment. These miRNA include described human miRNA miR-23a, -23b, -25, -188, -320, -363, -489, as well as mouse and rat miRNA homologous to miR-140*, mouse miR-329 and a novel miRNA, abi-13268. miRNA arrays for cytokine-stimulated ASM cells were completed in duplicate from two different cultures to identify candidate miRNA for further study. Cultures were growth arrested for 48 hours and treated with 10 ng/ml IL-1β, TNFα, and IFNγ for 24 hrs. A comparison of miRNA expression under cytokine-stimulated and non-treated conditions from hybridized miRNA arrays was calculated as described.
2010-08-17 | E-GEOD-16587 | biostudies-arrayexpress
Project description:Expression data from asthmatic and healthy airway smooth muscle cells
| PRJNA267606 | ENA
Project description:Expression data from human bronchial airway smooth muscle (ASM) cells
| PRJNA152499 | ENA
Project description:The inflammatory response of human airway smooth muscle cells
| PRJNA193319 | ENA
Project description:miRNA expression in human tracheal smooth muscle
| PRJNA116147 | ENA
Project description:Airway smooth muscle cells were stimulated with conditioned medium from BEAS-2B cells in the absence (Control) or Inhibition of miR-210.
2020-06-18 | E-MTAB-9224 | biostudies-arrayexpress
Project description:We used microarrays to determine if miRNA expression in human airway smooth muscle cells is altered by a pro-inflammatory stimulus. A majority of the miRNAs on the array exhibited very low signal intensity. In ASM cells exposed to IL-1β, TNFα, and IFNγ, none of the miRNA expressed were significantly up-regulated with cytokine treatment. We did observe 11 miRNA down-regulated > 2-fold in both cultures with cytokine treatment. These miRNA include described human miRNA miR-23a, -23b, -25, -188, -320, -363, -489, as well as mouse and rat miRNA homologous to miR-140*, mouse miR-329 and a novel miRNA, abi-13268.
2009-07-22 | GSE16587 | GEO
Project description:Human airway smooth muscle cells were co-cultured with BEAS-2B epithelial cells (or Control). Airway smooth muscle RNA was extracted and sent for Illumina HT-12 micro-array to examine gene expression.
2020-04-30 | E-MTAB-9004 | biostudies-arrayexpress
Project description:Smooth muscle differentiation has been proposed to sculpt airway epithelial branches in mammalian lungs. Serum response factor (SRF) acts with its cofactor myocardin to promote the expression of contractile smooth muscle markers. However, smooth muscle cells exhibit a variety of phenotypes beyond contractile that are independent of SRF-myocardin-induced transcription. To determine whether airway smooth muscle exhibits phenotypic plasticity during embryonic development, we deleted Srf from the pulmonary mesenchyme. Srf-mutant lungs branch normally, and the mesenchyme exhibits normal cytoskeletal features and patterning. scRNA-seq revealed an Srf-null smooth muscle cluster wrapping the airways of mutant lungs that lacks contractile smooth muscle markers but retains many features of control smooth muscle. Srf-null airway smooth muscle exhibits a synthetic phenotype, compared to the contractile phenotype of wildtype airway smooth muscle. Our findings reveal plasticity in mesenchymal differentiation during lung development and demonstrate that a synthetic smooth muscle layer is sufficient for airway branching morphogenesis.
2023-01-17 | GSE203171 | GEO