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.
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.
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.
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).
Project description:Generation of genome-wide maps of putative regulatory regions in human airway smooth muscle cells (ASMC) to aid in fine mapping of asthma GWAS. The cells were cultured and maintained in 10% FBS in PBS for 24 hours with no additional treatment given. MACS2 peaks provided in this submission were mapped to hg19.
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.
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.
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