Budesonide induced transcriptional activity in control and Gs-knockdown human airway smooth muscle cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE130715 | GEO | 2020/01/08
REPOSITORIES: GEO
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Project description:Budesonide induced transcriptional activity in control and Gs-knockdown human airway smooth muscle cells
| PRJNA541073 | ENA
Project description:Rationale. Lung inflammation in premature infants contributes to development of bronchopulmonary dysplasia (BPD), a chronic lung disease with long-term sequelae. Pilot studies administering budesonide suspended in surfactant have found reduced BPD without apparent adverse effects as occur with systemic dexamethasone therapy. Objectives. To determine effects of budesonide on differential genes expression in human fetal lung Methods. We prepared RNA from 3 samples of human fetal lung at 23 weeks gestation before (preculture, PC) and after 4 days culture as explants with (Bud) or without (Way) budesonide (30 nM) and performed RNAseq on the 9 samples.
2016-06-30 | E-GEOD-83888 | biostudies-arrayexpress
Project description:Inhaled corticosteroids (ICS) control airway inflammation in mild to moderate asthma by reducing inflammatory gene expression. However, incomplete understanding of the molecular mechanisms underpinning corticosteroid action hinders development of improved therapies for more severe disease. Microarray analysis was performed on RNA from biopsies taken from healthy individuals after receiving single dose of ICS to characterize corticosteroid-induced modulation of gene expression in the human airways. Healthy male, non-smoker, non-allergic volunteers (age 18-50 years) with normal lung function were recruited into a prospective, double-blind, placebo-controlled, randomized, two-period crossover study involving an initial screening visit, followed by two intervention visits. Participants were screened at visit 1 for fulfilment of the study eligibility criteria. At visit 2, volunteers were randomized to receive inhaled budesonide (1600 µg) or placebo, both via Turbuhaler. Two to three weeks later, at visit 3, participants received either budesonide or placebo, as appropriate to complete both study arms. Six hours after placebo or a budesonide inhalation, bronchial biopsies were obtained via bronchoscopy.
2016-06-11 | E-GEOD-83233 | biostudies-arrayexpress
Project description:Rationale. Lung inflammation in premature infants contributes to development of bronchopulmonary dysplasia (BPD), a chronic lung disease with long-term sequelae. Pilot studies administering budesonide suspended in surfactant have found reduced BPD without apparent adverse effects as occur with systemic dexamethasone therapy. Objectives. To determine effects of budesonide on differential genes expression in human fetal lung
2016-06-30 | GSE83888 | GEO
Project description:Background: Intratracheal budesonide mixed with surfactant has been investigated as an alternative to decrease lung injury and prevent bronchopulmonary dysplasia in preterm infants. However, possible systemic effects are not known. Our goal was identify systemic effects of intra-tracheal instilled budesonide by transcriptome analysis of the brain and lung in a preterm lamb model of mechanical ventilation. Methods: We performed RNA-sequencing of the fetal periventricular white matter and liver from preterm sheep after treatment with intratracheal budesonide mixed with surfactant or surfactant alone followed by mechanical ventilation. Unventilated animals were used as controls. mRNA profiles were generated from polyA selected RNA using Illumina platform. Read sequences were aligned to the sheep genome (Oar 4.0) using Bowtie2 followed read counts using featureCounts. We performed differential expression analysis using EdgeR. Results: We identified large and significant gene expression genes both in the liver and in the priventricular white matter in animals treated with budesonide+surfactant compared to surfactant alone and unventilated animals. There were complexes synergies and antagonism of effect of ventilation and budesonide on gene expression. Ventilation induced inflammatory signaling in the periventricular white matter and liver which was partially antagonized by budesonide. Budesonide also suppressed developmental pathways in the periventricular white matter. Conclusions: Intratracheal budesonide had systemic effects including suppression of developmental pathways in the brain. These effects could have clinical implication in affecting the neurodevelopmental outcomes of preterm newborns.
2019-11-26 | GSE131195 | GEO
Project description:Comparison of gene expression between Xist KO germ line stem GS cells and wildtype GS cells
2013-12-01 | GSE46589 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy with aggressive metastatic phenotype and very poor clinical prognosis. Interestingly, a lower occurrence of PDAC has been described in individuals with severe and long-standing asthma. Here we gained insight into the potential link between the glucocorticoid (GC) budesonide, a first-line therapy to treat asthma, and PDAC development. We found that in classical 2D setting, budesonide, but not classical GCs, used at high micromolar concentrations, modifies the behavior of PDAC cells, reducing their mesenchymal invasive/migrating features, without altering their proliferation or survival. However, a more physiological 3D environment drives PDAC cells towards a general metabolic reprogramming, which involves protein, lipid, and energy metabolism (e.g., increased glycolysis dependency). Remarkably, this metabolic change sensitizes PDAC cells to an unexpected anti-proliferative action of budesonide, which instead induces opposite metabolic changes (e.g., increased OXPHOS). Under these conditions, budesonide, as dexamethasone and hydrocortisone, inhibits PDAC spheroid growth and proliferation at nanomolar concentrations, in a GR-dependent manner, and through the induction of the tumor suppressor CDKN1C. Collectively, our study uncovers how the growth behavior/conditions influence the susceptibility of PDAC cells to glucocorticoids, and the tumor inhibitory action of budesonide in 3D condition (i.e., organotypic cultures, floating spheroids, and in vivo tumors). Validation in other cancer cells will be necessary to broaden the role of 3D setting and OXPHOS-to-glycolytic transition, in the induction of GC susceptibility. The inhibitory effect of budesonide on in vivo tumors suggests its potential suitability for clinical trials as a novel therapeutic approach to fight pancreatic cancer.
2025-01-02 | GSE255747 | GEO
Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy with aggressive metastatic phenotype and very poor clinical prognosis. Interestingly, a lower occurrence of PDAC has been described in individuals with severe and long-standing asthma. Here we gained insight into the potential link between the glucocorticoid (GC) budesonide, a first-line therapy to treat asthma, and PDAC development. We found that in classical 2D setting, budesonide, but not classical GCs, used at high micromolar concentrations, modifies the behavior of PDAC cells, reducing their mesenchymal invasive/migrating features, without altering their proliferation or survival. However, a more physiological 3D environment drives PDAC cells towards a general metabolic reprogramming, which involves protein, lipid, and energy metabolism (e.g., increased glycolysis dependency). Remarkably, this metabolic change sensitizes PDAC cells to an unexpected anti-proliferative action of budesonide, which instead induces opposite metabolic changes (e.g., increased OXPHOS). Under these conditions, budesonide, as dexamethasone and hydrocortisone, inhibits PDAC spheroid growth and proliferation at nanomolar concentrations, in a GR-dependent manner, and through the induction of the tumor suppressor CDKN1C. Collectively, our study uncovers how the growth behavior/conditions influence the susceptibility of PDAC cells to glucocorticoids, and the tumor inhibitory action of budesonide in 3D condition (i.e., organotypic cultures, floating spheroids, and in vivo tumors). Validation in other cancer cells will be necessary to broaden the role of 3D setting and OXPHOS-to-glycolytic transition, in the induction of GC susceptibility. The inhibitory effect of budesonide on in vivo tumors suggests its potential suitability for clinical trials as a novel therapeutic approach to fight pancreatic cancer.
2025-01-02 | GSE255746 | GEO
Project description:DNA hybridizations to compare genomic content of 11168-gs (genome-sequenced) to 11168-o (original) The genome sequence of the enteric bacterial pathogen Campylobacter jejuni NCTC 11168 (11168-GS) was published in 2000, providing a valuable resource for the identification of C. jejuni-specific colonization and virulence factors. Surprisingly, the 11168-GS clone was subsequently found to colonize 1-day-old chicks following oral challenge very poorly compared to other strains. In contrast, we have found that the original clinical isolate from which 11168-GS was derived, 11168-O, is an excellent colonizer of chicks. Other marked phenotypic differences were also identified: 11168-O invaded and translocated through tissue culture cells far more efficiently and rapidly than 11168-GS, was significantly more motile, and displayed a different morphology. Serotyping, multiple high-resolution molecular genotyping procedures, and subtractive hybridization did not yield observable genetic differences between the variants, suggesting that they are clonal. However, microarray transcriptional profiling of these strains under microaerobic and severely oxygen-limited conditions revealed dramatic expression differences for several gene families. Many of the differences were in respiration and metabolism genes and operons, suggesting that adaptation to different oxygen tensions may influence colonization potential. This correlates biologically with our observation that anaerobically priming 11168-GS or aerobically passaging 11168-O caused an increase or decrease, respectively, in colonization compared to the parent strain. Expression differences were also observed for several flagellar genes and other less well-characterized genes that may participate in motility. Targeted sequencing of the sigma factors revealed specific DNA differences undetected by the other genomic methods An all pairs experiment design type is where all labeled extracts are compared to every other labeled extract. Keywords: all_pairs
2005-12-31 | GSE3954 | GEO
Project description:Comparison of gene expression between Xist KO germ line stem GS cells and wildtype GS cells The gene expression of GS cells derived from postnatal mouse testis was investigated. RNA from Xist KO-, wildtype-GS cells, and ES cells were used for this study. 3 independent samples from each cell line were used.
2013-12-01 | E-GEOD-46589 | biostudies-arrayexpress