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Effect of TGF-beta1 on the miRNome in CFBE41o- cells stably transduced with Wild Type (WT)-CFTR and F508del-CFTR

ABSTRACT: Effect of TGF-beta1 on the miRNome in CFBE41o- cells stably transduced with Wild Type (WT)-CFTR and F508del-CFTR

PROVIDER: PRJNA528815 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8775940.fastq.gz	Fastqsanger.gz
	SRR8775941.fastq.gz	Fastqsanger.gz
	SRR8775942.fastq.gz	Fastqsanger.gz
	SRR8775943.fastq.gz	Fastqsanger.gz
	SRR8775944.fastq.gz	Fastqsanger.gz

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

Project description:The purpose of this study was to explore baseline expression of miRNome in Cystic Fibrosis Bronchial Epithelial (CFBE41o-) cells stably transfected with wild type (WT) Cystic Fibrosis Transmembrane Conductance regulator (CFTR) and F508del-CFTR. To fulfill this goal miRNA sequencing was done to see miRNA landscape in CFBE41o- Cells with homozygous F508del mutated CFTR and in CFBE41o- Cells with homozygous WT-CFTR, without any treatment condition.

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Effect of TGF-beta1 on the miRNome in CFBE41o- cells stably transduced with Wild Type (WT)-CFTR and F508del-CFTR

Project description:The purpose of this study was to explore miRNA mediated Transforming Growth Factor (TGF)-β1 regulation of F508del Cystic Fibrosis Transmembrane Conductance regulator (CFTR). To fulfill this goal, miRNA sequencing was done to see miRNA landscape in Cystic Fibrosis Bronchial Epithelial (CFBE) Cells with homozygous WT-CFTR and F508del mutated CFTR in response to TGFβ1 treatment.

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

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

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ATACseq of CFBE41o- stably expressing wild-type CFTR (WTBE) and F508del-CFTR (CFBE) cells

Project description:ATACseq of CFBE41o- stably expressing wild-type CFTR (WTBE) and F508del-CFTR (CFBE) cells

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Multi-omics comparisons between CFBE41o- cells stably expressing wide-type CFTR and F508del-mutant CFTR

Project description:Multi-omics comparisons between CFBE41o- cells stably expressing wide-type CFTR and F508del-mutant CFTR

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ATACseq of CFBE41o- stably expressing wild-type CFTR (WTBE) and F508del-CFTR (CFBE) cells

Project description:Cystic fibrosis (CF) is characterized by chronic inflammation and excessive cytokines secretion in the lung. Isogenic human CF bronchial epithelial (CFBE41o-) cell lines stably expressing wt-CFTR (WTBE) or F508del mutant (CFBE) are widely used tools in understanding responses to stimuli or drugs and CF pathogenesis in vitro. However, their intrinsic cellular differences in culture are unknown. Hence, we performed integrative analyses at protein, mRNA and chromatin levels on these isogenic cell lines cultured in submerged and transwell condition. CFBE and WTBE cells displayed different secretion patterns on IL-6, IL-8, CXCL1, CXCL10, and CCL5 . The ALI culture dramatically increased cytokines secretion in both cells. ATAC-seq results showed that CFBE cells exhibited higher genome-wide chromatin accessibility than WTBE cells in both culture methods, but the relative openness of cytokine genes between two cells varied individually. Differentially expressed genes between two cell lines from mRNA sequencing were highly concentrated in immunity-related pathways. While the mRNA stability of CXCL10 and CXCL1 exhibited the most significant differences between cell lines in SUB culture, most cytokines had comparable mRNA stabilities within same culture method. Moreover, polarization of cells via transwell culture remodeled the chromatin accessibility and transcriptome. This multilayered studies presents a comprehensive baseline activities of CFBE and WTBE cells, further facilitating their usage and data interpretation as CF cell models.

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

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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

Multi-omics comparisons between CFBE41o- cells stably expressing wide-type CFTR and F508del-mutant CFTR

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-01 | GSE186920 | GEO

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

Project description:Whole transcriptional analysis of normal 16HBE14o- cells, cystic fibrosis (CF) patients-derived CFBE41o- cells, and WT-CFTR-rescued CFBE41o- cells. We utilized the gene expression data to understand the transcriptional regulation underlying the loss of CFTR function.

2019-01-31 | GSE110289 | GEO

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