The effect of apolipoprotein E on asthmatic bronchial brushing cell gene signature
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ABSTRACT:
PROVIDER: PRJNA527849 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8747490.fastq.gz | Fastqsanger.gz | |||
| SRR8747490_1.fastq.gz | Fastqsanger.gz | |||
| SRR8747490_2.fastq.gz | Fastqsanger.gz | |||
| SRR8747491.fastq.gz | Fastqsanger.gz | |||
| SRR8747491_1.fastq.gz | Fastqsanger.gz |
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Project description:Human asthmatic bronchial brushing cells stimulated with apolipoprotein E demonstrate increased expression of mRNA transcripts encoding multiple pro-inflammatory genes
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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: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: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: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:Obese asthma is a chronic disease that poses a serious threat to children's health, resulting in more severe wheezing, earlier airway remodelling, and insensitivity to hormone therapy. Despite its clinical importance, knowledge on the underlying mechanisms of this disease remains limited. This study aimed to elucidate the pathogenesis of obese asthmatic utilizing a murine model. The present study randomly divided thirty female BALB/c mice into three groups: normal mice, asthmatic mice, and obese asthmatic mice. The mice were fed a with high-fat diet (HFD) to induce obesity. Asthmatic mice were subjected to ovalbumin (OVA) sensitization and challenge. Mice with obesity were then subjected to OVA sensitization and challenge to develop obese asthmatic. Airway remodelling was observed in obese asthmatic mice. Proteomic and bioinformatics analyses were conducted on lung tissues from obese asthmatic and normal mice. A total of 200 proteins were differentially expressed in obese asthmatic compared to normal mice; of these, 53% were upregulated and 47% were downregulated. Pathway analysis revealed that obese asthmatic primarily affected the lysosome, phagosome, and sphingolipid metabolism pathways. In addition, pyroptosis was observed in obese asthmatic, along with significant increases in pyroptosis-related factors. Orosomucoid like 3 (ORMDL3), NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and Gasdermin-D (GSDMD) expression was examined, with particularly high expression levels observed in obese asthmatic mice. In vitro experiments demonstrated that overexpression of ORMDL3 in human bronchial epithelial (HBE) cells led to increased expression of NLRP3, GSDMD, and cathepsin D (CTSD). These findings suggest that ORMDL3 may regulate pyroptosis and subsequent airway remodelling in obese asthmatic, possibly via CTSD/NLRP3/GSDMD pathway.
2023-07-07 | PXD043630 |
Project description:Human Rhinovirus (HRV) infection can trigger exacerbations of asthma. Understanding of the mechanisms provoking airway inflammation and remodeling in asthma, as well as the pathogenic mechanisms of HRV infection and its association with asthma exacerbations, may offer significant opportunities for improved disease management. Genome-wide expression analysis of HRV type 1A-infected primary bronchial epithelial (PBE) cells from normal and asthmatic donors was performed to determine whether asthma is associated with a unique pattern of gene expression after HRV infection in vitro. Experiment Overall Design: Frozen stocks of human PBE cells obtained from the bronchial brushings of six normal and five asthmatic individuals were grown in vitro in Bronchial Epithelial Growth Media (BEGM, Lonza). Subconfluent monolayers of PBE cells were infected with purified and concentrated minor group HRV serotype 1A at multiplicity of infection of 10 plaque forming units (pfu) per cell or mock-infected with growth media alone. Cells were lysed 16 hours post infection (p.i.) and isolated total RNAs were analyzed using the Human Genome U133 Plus 2.0 GeneChip arrays (Affymetrix, Santa Clara, CA).
2008-11-13 | E-GEOD-13396 | biostudies-arrayexpress
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:mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy and nasal epithelial cells collected by brushing the inferior turbinate from healthy current and never smoker volunteers in order to determine the relationship between smoking-related gene expression changes in bronchial and nasal epithelium within the same individual.
2011-03-14 | GSE16008 | GEO
Project description:The airway epithelium forms the interface between the inhaled environment and the lung. The airway epithelium is dysfunctional in asthma and epigenetic mechanisms are considered a contributory factor. We hypothesised that the DNA methylation profiles of cultured primary airway epithelial cells (AECs) would differ between cells isolated from individuals with asthma (n=17) versus those without asthma (n=16). AECs were isolated from patients by two different isolation techniques; pronase digestion (9 non-asthmatic, 8 asthmatic) and bronchial brushings (7 non-asthmatic and 9 asthmatic). DNA methylation was assessed using an Illumina Infinium HumanMethylation450 BeadChip array. DNA methylation of AECs clustered by isolation technique and linear regression identified 111 CpG sites differentially methylated between isolation techniques in healthy individuals. As a consequence, the effect of asthmatic status on DNA methylation was assessed within AEC samples isolated using the same technique. In pronase isolated AECs, 15 DNA regions were differentially methylated between asthmatics and non-asthmatics. In bronchial brush isolated AECs, 849 differentially methylated DNA regions were identified with no overlap to pronase regions. In conclusion, regardless of cell isolation technique, differential DNA methylation was associated with asthmatic status in AECs, providing further evidence for aberrant DNA methylation as a signature of epithelial dysfunction in asthma.
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