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Gene expression data in linc-SUMF1-2 knockdown human bronchial epithelial cells

ABSTRACT: Whole transcriptional analysis of cystic fibrosis (CF) patients-derived CFBE41o- cells under the linc-SUMF1-2 knockdown condition. We utilized the gene expression data to understand the linc-SUMF1-2 function in CF bronchial epithelial cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110288 | GEO | 2019/01/31

REPOSITORIES: GEO

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Gene expression data from human bronchial epithelial cell lines: comparison between normal and CFTR-deficient cells

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2019-01-31 | GSE110289 | GEO

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Transcriptional profiling of CFBE41o-ΔF508 cells and CFBE41o−CFTR cells.

Project description:Cystic fibrosis bronchial epithelial (CFBE41o-ΔF508) cells subjected to 23 bio-active small molecules including vehicle controls, at low temperature and untreated cells. Untreated Cystic fibrosis bronchial epithelial cells (CFBE41o−CFTR) are also included.

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Influence of inflammation on the expression and activity of glycosyltransferases in human bronchial mucosa

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The miRNome in CFBE41o- cells stably transduced with F508del-CFTR and WT-CFTR

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Influence of inflammation on the expression and activity of glycosyltransferases in human bronchial mucosa

Project description:Bronchial inflammation is common in patients suffering from Cystic Fibrosis (CF) and is commonly responsible for mortality from CF. It is known that this inflammation has an influence over glycosylation events in bronchial mucins and abnormal glycosylation has been described in CF. These abnormalities can not be directly linked to CF, as the cells that secrete bronchial mucins do not express CFTR. This study is to determine if bronchial inflammation could be responsible for abnormal glycoslylation in CF. Pro-inflammatory cytokines TNF, IL6, and IL8, as well as anti-inflammatory cytokine IL10 are present and seem to have active roles in the respiratory tree of CF patients. In this study, the effects of these cytokines on the expression of glycosyl- and sulfotransferases involved in the biosynthesis of O-glycans in the bronchial cell line Calu-3 were analyzed. Three replicates for each cytokine treated group and controls were hybridized to GLYCOv2 array.

2011-03-02 | E-GEOD-27594 | biostudies-arrayexpress

THE PHARMACOLOGICAL RESCUE OF CFTR BY LUMACAFTOR (VX-809) IN THE CYSTIC FIBROSIS BRONCHIAL EPITHELIUM IS ASSOCIATED WITH AN EXTENSIVE REORGANIZATION OF MITOCHONDRIA.

Project description:Cystic Fibrosis (CF) is a genetic disorder CF is caused by mutations of the gene encoding for the cystic fibrosis transmembrane conductance regulator protein (CFTR), a transmembrane anion channel expressed at the apical membrane of several organs, including the epithelial cells of the airway. CFTR mutations result in dysfunctional ion transport across the apical membrane at the surface of the epithelia, generating thickened and dehydrated secretions. In the lung, this leads to a decrease in the mucociliary clearance, favoring bacterial colonization and progressive obstruction of the duct. Although over 2000 CFTR variants have been identified so far, the most common mutation is a deletion of the phenylalanine in position 508 (F508del), which shows an allelic frequency of around 90% among CF patients. F508del-CFTR is incorrectly folded, causing its retention at the endoplasmic reticulum (ER) and subsequent proteasomal degradation. Among the several drugs available in CF pharmacological treatment, VX-809 (commercial name Lumacaftor) is the most used drug for patients carrying F508del-CFTR mutation. This drug corrects the aberrant folding of F508del-CFTR by favoring the correct intramolecular interactions, thus enabling a higher number of copies of the defective protein to reach the plasma membrane. We applied SWATH-based proteomics to understand if a pharmacological rescue of F508del-CFTR is associated with changes in global protein expression of the human bronchial epithelium by using the CFBE41o- cell model, a line that stably expresses F508del-CFTR.

2022-08-11 | PXD028355 | Pride

Exploring intrinsic variability between cultured nasal and bronchial epithelia in cystic fibrosis

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Expression data from human bronchial epithelial cells

Project description:The F508del mutation, the most frequent in cystic fibrosis (CF), impairs the maturation of the CFTR chloride channel. The F508del defect can be partially overcome at low temperature (27 Â°C) or with pharmacological correctors. The rescue elicited by low temperature may involve a direct stabilization of mutant CFTR protein and/or a change in cell transcriptome that creates a more favorable proteostasis environment. To assess the effect of low temperature on gene expression we investigated the transcriptome of bronchial epithelial cells derived from CF with F508del mutation. Cells were kept under control conditions or incubated at 27 Â°C. Microarray data indicate that hypothermia induces a profound and global change in gene expression that may be in part responsible for rescue of F508del-CFTR. Bronchial epithelial cells from cystic fibrosis patients homozygotes for F508del mutation were isolated. Cells differentiated as epithelial monolayers on porous membranes (Snapwell inserts) were incubated for 24 hours at 27 Â°C or kept under control conditions. Rescue of mutant CFTR channel by low temperature was checked by measuring transepithelial chloride currents with the Ussing chamber technique. Total RNA was extracted from treated and control cells to assess changes in gene expression with microarrays.

2016-07-01 | E-GEOD-70442 | biostudies-arrayexpress

THE PROTEOME SPECIATION OF AN IMMORTALIZED CYSTIC FIBROSIS CELL LINE: NEW PERSPECTIVES ON THE PATHOPHYSIOLOGY OF THE DISEASE.

Project description:Cystic Fibrosis (CF) is a recessively inherited disease caused by mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. CFTR has a pivotal role in the onset of CF, and several proteins are directly or indirectly involved in its homeostasis. To study these CFTR interactors at protein species level, we used a functional proteomics approach combining 2D-DIGE, mass spectrometry and enrichment analysis. A human cystic fibrosis bronchial epithelial cell line (CFBE41o-) was used for analysis. 74 differentially expressed spots were identified and some were validated by western-blot. Enrichment analysis highlighted molecular pathways in which ezrin, HSP70, endoplasmin and lamin A/C, in addition to CFTR, were considered central hubs in CFTR homeostasis. These proteins acquire different functions through post-translational modifications, emphasizing the importance of studying the CF proteome at protein species level. Moreover, serpin H1, prelamin A/C, protein-SET and cystatin-B were associated for the first time to CF, demonstrating the importance of heat shock response, cross-talk between the cytoskeleton and signal transduction, chronic inflammation and alteration of CFTR gating in the pathophysiology of the disease. These results open new perspectives for the understanding of the proteostasis network, characteristic of CF pathology, and could provide a springboard for new therapeutic strategies.

2022-03-01 | PXD006933 | Pride

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