Genome-wide gene methylation study in primary cultured airway smooth muscle cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA610277 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We generated genome-wide methylation data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide expression data from the same individuals.
2020-03-30 | GSE146376 | GEO
Project description:We generated genome-wide expression data from primary cultured airway smooth muscle cells (ASMCs) exposed to IL-13, IL-17, IL-13+IL-17, and vehicle. This data was generated in combination with genome-wide methylation data from the same individuals.
2020-03-30 | GSE146374 | GEO
Project description:Genome-wide gene expression study in primary cultured airway smooth muscle cells
| PRJNA610276 | ENA
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:Glucocorticoids, which activate glucocorticoid receptor signaling and thus modulate gene expression, are widely used to treat asthma. Glucocorticoids exert their therapeutic effects in part through modulating airway smooth muscle structure and function. However, the effects of genes that are regulated by GCs on airway function are not fully understood. Here, we used transcription profiling to characterize the effects of a potent glucocorticoid, dexamethasone, on cultured human airway smooth muscle gene expression at 4 and 24 hours. This study examined differential gene expression induced by treatment of cultured human airway smooth muscle cells with dexamethasone. There were 3 groups of samples and each group had 4 biological replicates. Group 1 was no treatment, Group 2 was dexamethasone (dex) treatment for 4 hours, Group 3 was dex treatment for 24 hours. Cultures were synchronized so harvest occurred at the same time for all three groups. 2 samples are not included in this analysis (based on unsupervised clustering of samples and diagnostic plots).
2011-12-10 | E-GEOD-34313 | biostudies-arrayexpress
Project description:Glucocorticoids, which activate glucocorticoid receptor signaling and thus modulate gene expression, are widely used to treat asthma. Glucocorticoids exert their therapeutic effects in part through modulating airway smooth muscle structure and function. However, the effects of genes that are regulated by GCs on airway function are not fully understood. Here, we used transcription profiling to characterize the effects of a potent glucocorticoid, dexamethasone, on cultured human airway smooth muscle gene expression at 4 and 24 hours.
2011-12-10 | GSE34313 | GEO
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
Project description:Genome-wide gene expression and methylation studies in primary cultured airway smooth muscle cells
| PRJNA610275 | ENA
Project description:Persistent severe asthma is associated with hyper-contractile airways and structural changes in the airway wall, including an increased airway smooth muscle (ASM) mass. This study used gene expression profiles from asthmatic and healthy airway smooth muscle cells grown in culture to identify novel receptors and pathways that potentially contributed to asthma pathogenesis. We used microarrays to compare the gene expression between asthmatic and healthy airway smooth muscle cells to understand the underlying pathway contributing the differences in cellular phenotypes
2015-01-31 | GSE63383 | GEO
Project description:Selective stimulation of IL-4 receptor on smooth muscle induces airway hyper-responsiveness in mice. Abstract: Production of the cytokines IL-4 and IL-13 is increased in both human asthma and mouse asthma models and Stat6 activation by the common IL-4/IL-13R drives most mouse model pathophysiology, including airway hyperresponsiveness (AHR). However, the precise cellular mechanisms through which IL-4Rα induces AHR remain unclear. Overzealous bronchial smooth muscle constriction is thought to underlie AHR in human asthma, but the smooth muscle contribution to AHR has never been directly assessed. Furthermore, differences in mouse vs. human airway anatomy and observations that selective IL-13 stimulation of Stat6 in airway epithelium induces murine AHR raise questions about the importance of direct IL-4R effects on smooth muscle in murine asthma models and relevance of these models to human asthma. Using transgenic mice in which smooth muscle is the only cell type that expresses or fails to express IL-4Rα, we demonstrate that direct smooth muscle activation by IL-4, IL-13, or allergen is sufficient, but not necessary, to induce AHR and show that 5 genes known to promote smooth muscle migration, proliferation and contractility are activated by IL-13 in smooth muscle in vivo. These observations demonstrate that IL-4Rα promotes AHR through multiple mechanisms and provide a model for testing smooth muscle-directed asthma therapeutics. For the microarray aspect of of the study, there were three groups of mice: 1. IL4R gene knockout (KO) mice 2. WT mice 3. IL4R KO mice that were also transgenic for a gene construct that expressed IL4R under the control of the smooth muscle-specific promoter from the SMP8 gene All mice were subjected to intratracheal IL13 exposure for 7 days, and whole lung RNA was prepared for microarray analysis 24 hours after the last instillation. Per treatment and genotype: Two RNA pools were made from four mice each. These were labeled and hybridized to make a total of 6 microarrays. RNA was labeled with the standard Affymetrix 3' labeling protocol to make cDNA that was hybridized to Mouse MOE 430 plus 2.0 GeneChips. Gene transcripts were identified that differed in their relative expression as a function of IL4R expression on the smooth muscle cells.
2011-01-07 | E-GEOD-26476 | biostudies-arrayexpress