Single-cell RNA-seq profiling of human bronchial epithelial preparations from non-CF and CF samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE335566 | GEO | 2026/08/04
REPOSITORIES: GEO
Similar Datasets
Project description:We did bulk RNA sequencing in newborn cystic fibrosis (CF) and non-CF pig kidney. We compared kidney gene expression profiling between non-CF and CF pigs. RNA sequencing results showed that there is not significant difference between non-CF and CF in terms of gene expression, suggesting that CFTR knockout does not affect kidney development in newborn pigs.
2024-06-07 | GSE217122 | GEO
Project description:Single-cell RNA-seq profiling of human bronchial epithelial preparations from non-CF and CF samples
| PRJNA1478899 | ENA
Project description:Cystic fibrosis (CF), a genetic disorder, is characterized by chronic lung disease. Small non-coding RNAs are key regulators of gene expression and participate in various processes, which are dysregulated in CF; however, they remain poorly studied. Here, we determined the complete microRNAs (miRNAs) expression pattern in three CF ex-vivo models. The miRNA profiles of air-liquid interface cultures of airway epithelia (bronchi, nasal cells, and nasal polyps) samples from patients with CF and non-CF controls were obtained by deep sequencing. Compared with non-CF controls, several miRNAs were deregulated in CF samples, for instance miR-181a-5p and the miR-449 family were upregulated. Moreover, mature miRNAs often showed variations (i.e., isomiRs) relative to their reference sequence, such as miR-101, suggesting that miRNAs consist of heterogeneous repertoires of multiple isoforms with different effects on gene expression. Analysis of miR-181a-5p and miR-101-3p roles indicated that they regulate the expression of WISP1, a key component of cell proliferation/migration programs. We showed that miR-101 and miR-181a-5p participated in aberrant recapitulation of wound healing programs by controlling WISP1 mRNA and protein level. Our miRNA expression data bring new insights into CF physiopathology and define new potential therapeutic targets in CF
2020-10-21 | GSE159708 | GEO
Project description:Cystic Fibrosis (CF) is associated with pathology in multiple tissues including the lung, digestive tract and reproductive system. Lung disease is primarily a post-natal event but other organs are affected before birth. Here we use the CF sheep model to investigate the initiation and progression of CF disease through gestation.
2023-02-14 | GSE202024 | GEO
Project description:We have compared gene expression in human nasal brushing cells from 19 cystic fibrosis (CF) patients and 19 healthy controls using a 5.2K cDNA microarray. Our aim is to identify new disease biomarkers for the Cystic Fibrosis Gene Therapy Consortium. These markers will be used to report more effectively on the response to the administration of gene therapy in vivo. Cystic Fibrosis is a recessive genetic disease caused by mutations in the cystic fibrosis conductance regulator (CFTR) gene which encodes a chloride ion channel. The most common mutation is the ∆F508 mutation, present on 70% of CF chromosomes in Caucasian populations. The disease affects many organs in the body such as the pancreas, liver, sweat glands, small intestine and reproductive tracts but is most commonly associated with progressive, inflammatory lung disease. The current average life expectancy of CF patients is 35 years. Gene therapy is being developed as a treatment for CF airway disease, however, means of measuring the efficiency and efficacy of gene therapy in vivo are lacking. This is mainly due to the difficulty in measuring the chloride conductance of CFTR in cells and tissues. Furthermore, clinical assays for measuring improvements in lung function are insensitive. Surrogate markers of inflammation and CFTR function will therefore be important for the effective assessment of gene therapy in vivo. We have analysed gene expression in human nasal epithelium as this is considered an accessible surrogate for the conducting airways where disease manifests in the majority of patients. Additionally, this tissue will be sampled in clinical trials.
2011-04-30 | E-MEXP-436 | biostudies-arrayexpress
Project description:To provide a more detailed survey of adaptive changes in the physiology of P. aeruginosa (PA) during long-term infection of the cystic fibrosis (CF) lung, we performed a comparative proteome and transcriptome analysis of a set of isogenic sequential non-mutator and mutator isolates from three selected CF patients. Recently, we showed that during CF lung persistence PA mutators converge to a virulence-attenuated phenotype. In this study, we demonstrate that besides virulence-associated traits (VATs) the adaptation process of PA predominantly comprises metabolic pathways. In end-stage mutator strains, transcripts of genes encoding VATs, chemotaxis, degradation of aromatic compounds and several two-component regulatory systems were decreased. In contrast, several transcripts of genes or proteins involved in metabolism of fatty acids, nucleotides, amino acids and the generation of energy were increased. Of particular interest is the increased expression level of genes involved in (i) the anaerobic arginine-deiminase pathway, (ii) the anaerobic respiration such as nitrate-uptake protein OprF, redox-active azurin and cytchrome c551 peroxidase, (iii) the micro-aerobic respiration such as high oxygen-affinity cytochrome oxidase cbb3 (iv) the tricarboxylic acid cycle (TCA), glyoxylate shunt and anaplerotic carboxylation reactions to oxaloacetate. Strikingly, an increased transcription of the anaerobic regulator gene anr correlates with the up-regulation of ANR-dependent genes. In conclusion, these changes in transcriptome and proteome indicate an adaptive shift towards constitutive expression of genes of metabolic pathways obviously required for growth under micro-aerobic and nutritional conditions of suppurative CF lung tissue. Finally, these results provide us with new targets for antimicrobial agents and biomarkers reflecting adaptation of PA towards progressive CF lung disease. Experiment Overall Design: P. aeruginosa isolates recovered from different time points of chronic cystic fibrosis lung disease were cultered in vitro, harvested for RNA extraction and hybridization on Affymetrix microarrays. We compared the transcriptome (triplicate microarrays) of early non-mutator P. aeruginosa isolates with late mutator isolates with high mutation frequency probably the driving force of an efficient adaptation to changing environements to conclude from differences in gene expression to the requirements of CF lung environment. Experiment Overall Design: Second publication of array data to be added later
2009-06-08 | E-GEOD-10362 | biostudies-arrayexpress
Project description: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.
2019-01-31 | GSE110288 | GEO
Project description:Chronic Pseudomas aeruginosa infection in the lung is a common in people with cystic fibrosis (CF). Current therapies for CF fail to eliminate persistent bacterial infections, chronic inflammation, or irreversible lung damage. Our group engineered mesenchymal stromal cell (MSC)-derived extracellular vesicles (EVs) to carry the microRNA let-7b-5p as a dual anti-infective and anti-inflammatory treatment. In a preclinical CF mice model, we found that let-7b-5p-loaded MSC EVs reduced P. aeruginosa burden, immune cells and proinflammatory cytokines in the lungs. This research hypothesized two mechanisms of the observed effects in the mouse model: anti-inflammatory properties of the let-7b-5p-loaded MSC EVs and inhibition of antibiotic-resistant P. aeruginosa biofilm formation in CF airways. Primary human broncial epithelial cells (pHBECs) were exposed to P. aeruginosa and treated with differet MSC EV conditions. The results demonstrated that MSC EVs engineered to contain let-7b-5p effectively blocked the formation of P. aeruginosa biofilms on pHBECs while also reducing P. aeruginosa-induced inflammation by CF-pHBECs.
2025-06-16 | GSE295607 | GEO
Project description:The goal of this study was to examine changes in gene expression over time in healthy and cystic fibrosis (CF) human airway epithelia infected with RSV.
2023-11-08 | GSE247298 | GEO
Project description:Cystic Fibrosis Related Diabetes (CFRD), the main co-morbidity in Cystic Fibrosis (CF), is associated with higher rates of lung function decline. We hypothesize that airway epithelial barrier function is impaired in CF and is further exacerbated under hyperglycemia, worsening pulmonary outcomes. Using 16HBE cells as a model cell line, we studied the effects of hyperglycemia in airway epithelial barrier function. Results show increased paracellular dye flux in CF cells in response to insulin treatment under hyperglycemia, suggesting impaired barrier integrity. Gene expression experiments identified Claudin-4 (CLDN4) as a key tight junction protein dysregulated in CF cells. Further investigation into CLDN4 protein localization by confocal microscopy showed that CLDN4 was tightly localized at tight junctions in WT cells and localization did not change under hyperglycemia. ln contrast, CLDN4 was less well-localized in CF cells at normal glucose and localization was worsened in CF cells conditioned to hyperglycemia. Treatment with highly effective modulator compounds (ETI) reversed this trend, and CFTR rescue by ETI in CF cells was not affected by insulin treatment or hyperglycemia. Bulk RNA sequencing showed differences in transcriptional responses in CF compared to WT cells under normal or high glucose, highlighting PTPRG as a promising target for further investigation.
2024-06-03 | GSE268909 | GEO