MiRNA Analysis of lungs of LCPUFA-treated asthmatic C57BL/6 mice and respective controls
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ABSTRACT:
ORGANISM(S): Mus musculus synthetic RNA Homo sapiens
PROVIDER: GSE135597 | GEO | 2019/12/31
REPOSITORIES: GEO
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Project description:Rationale: Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from asthmatic children fail to heal a wound in vitro. Objectives: To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma. Methods: Airway epithelial cells (AEC) from children with asthma (n=36), healthy atopic (n=23) and healthy non-atopic controls (n=53) were investigated by microarray, gene expression and silencing, transcript regulation analysis and ability to close mechanical wounds. Results: Wound repair of AEC from healthy and atopic children were not significantly different and were both faster than AEC from asthmatics. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by qPCR and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in non-asthmatic AEC inhibited wound repair, while addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5â, 2âdeoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation. Conclusions: These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells. 16 arrays, 2 experimental groups, asthma atopic, AA, and healthy non-atopic, HN.
2010-04-12 | E-GEOD-18965 | biostudies-arrayexpress
Project description:Rationale: Damage to airway epithelium is followed by deposition of extracellular matrix (ECM) and migration of adjacent epithelial cells. We have shown that epithelial cells from asthmatic children fail to heal a wound in vitro. Objectives: To determine whether dysregulated ECM production by the epithelium plays a role in aberrant repair in asthma. Methods: Airway epithelial cells (AEC) from children with asthma (n=36), healthy atopic (n=23) and healthy non-atopic controls (n=53) were investigated by microarray, gene expression and silencing, transcript regulation analysis and ability to close mechanical wounds. Results: Wound repair of AEC from healthy and atopic children were not significantly different and were both faster than AEC from asthmatics. Microarray analysis revealed differential expression of multiple gene sets associated with repair and remodeling in asthmatic AEC. Fibronectin (FN) was the only ECM component whose expression was significantly lower in asthmatic AEC. Expression differences were verified by qPCR and ELISA, and reduced FN expression persisted in asthmatic cells over passage. Silencing of FN expression in non-asthmatic AEC inhibited wound repair, while addition of FN to asthmatic AEC restored reparative capacity. Asthmatic AEC failed to synthesize FN in response to wounding or cytokine/growth factor stimulation. Exposure to 5’, 2’deoxyazacytidine had no effect on FN expression and subsequent analysis of the FN promoter did not show evidence of DNA methylation. Conclusions: These data show that the reduced capacity of asthmatic epithelial cells to secrete FN is an important contributor to the dysregulated AEC repair observed in these cells.
2010-03-31 | GSE18965 | GEO
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.
2021-06-10 | PXD015566 | Pride
Project description:miRNA Analysis of lungs of LCPUFA-treated asthmatic C57BL/6 mice and respective controls
| PRJNA559388 | ENA
Project description:Airway inflammation is the hallmark of asthma and suggests a dysregulation of homeostatic mechanisms. MicroRNAs (miRNAs) are key regulators of gene expression, necessary for the proper function of cellular processes. We used miRNA microarrays to compare the profiles of human bronchial epithelial cells from healthy and asthmatic donors Human bronchial epithelial cells were isolated from healthy and asthmatic donors. RNA was extracted and miRNA expression was analyzed on Affymetrix miRNA microarrays. We sought to utilize miRNA expression as a tool for understanding underlying biological differences in BECs from healthy and asthmatic donors.
2012-10-31 | E-GEOD-25230 | biostudies-arrayexpress
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.
2023-05-02 | PXD015604 | Pride
Project description:Airway inflammation is the hallmark of asthma and suggests a dysregulation of homeostatic mechanisms. MicroRNAs (miRNAs) are key regulators of gene expression, necessary for the proper function of cellular processes. We used miRNA microarrays to compare the profiles of human bronchial epithelial cells from healthy and asthmatic donors
2012-10-31 | GSE25230 | GEO
Project description:Background: Aberrant expression of small non-coding RNAs (sncRNAs), in particular microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs) define several pathological processes. Asthma is characterized by airway hyper-reactivity, chronic inflammation and airway wall remodeling. Asthma-specific miRNA profiles were reported for bronchial epithelial cells, but no information on sncRNA expression in asthmatic bronchial smooth muscle (BSM) cells is available. Objective: To determine whether primary BSM sncRNA expression profile is altered in asthma and identify targets of differentially expressed sncRNAs. Methods: SmallRNA sequencing was used for sncRNA profiling in BSM cells (8 asthma, 6 non-asthma). sncRNA identification and differential expression analysis was performed with iMir, . experimentally validated miRNA targets were identified with Ingenuity Pathway Analysis and putative piRNA targets with miRanda. Results: Asthmatic BSM cells showed abnormal expression of 32 sncRNAs (26 miRNAs, 5 piRNAs, and 1 snoRNA). Target prediction for deregulated miRNAs and piRNAs revealed experimentally validated and predicted mRNA targets expressed in the BSM cells. 38 of these mRNAs represent major targets for deregulated miRNAs and may play important roles in the pathophysiology of asthma. Interestingly, 6 such miRNAs were previously associated with asthma and/or considered as novel therapeutic targets for treatment of this disease. Signaling pathway analysis revealed involvement of these sncRNAs in increased cell proliferation via PTEN and PI3K/Akt signaling pathways. Conclusions: BSM cells from asthma patients are characterized by aberrant sncRNA expression that recapitulates multiple pathological phenotypes of these cells. Implications: sncRNA expression profiling performed in this study further improve our understanding of the molecular mechanisms underlying asthma-associated processes in lungs.
2018-01-07 | GSE64744 | GEO
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:Background The timing and mechanisms of asthma inception remain imprecisely defined. Although epigenetic mechanisms likely contribute to asthma pathogenesis, little is known about their role in asthma inception. Objective To assess whether the trajectory to asthma begins already at birth and epigenetic mechanisms, specifically DNA methylation, contribute to asthma inception. Methods We used a combination of methyl binding protein-dependent DNA capture and microarrays to survey DNA methylation in cord blood mononuclear cells (CBMC) from 36 children (18 non-asthmatic, 18 asthmatic by age 9) from the Infant Immune Study (IIS), an unselected birth cohort closely monitored for asthma for a decade. SMAD3 methylation in IIS (n=60) and in two replication cohorts (The Manchester Asthma and Allergy Study, n=30, and the Childhood Origins of ASThma Study, n=28) was analyzed by bisulfite sequencing or Illumina 450K arrays. CBMC-derived IL-1b was measured by ELISA. Results Neonatal immune cells harbored 589 differentially methylated regions (DMRs) that distinguished IIS children who did and did not develop asthma by age 9. In all three cohorts, methylation in SMAD3, the most connected hub within the network of asthma-associated DMRs, was selectively increased in asthmatic children of asthmatic mothers and was associated with childhood asthma risk. Moreover, SMAD3 methylation in IIS neonates with maternal asthma was strongly and positively associated with neonatal production of IL-1b, an innate inflammatory mediator. Conclusions The trajectory to childhood asthma begins at birth and involves epigenetic modifications in immunoregulatory and pro-inflammatory pathways. Maternal asthma influences epigenetic mechanisms that contribute to the inception of this trajectory.
2017-04-13 | GSE85228 | GEO