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Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia

ABSTRACT: Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia

PROVIDER: PRJNA673903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12967600_1.fastq.gz	Fastqsanger.gz
	SRR12967600_2.fastq.gz	Fastqsanger.gz
	SRR12967601_1.fastq.gz	Fastqsanger.gz
	SRR12967601_2.fastq.gz	Fastqsanger.gz
	SRR12967602_1.fastq.gz	Fastqsanger.gz

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Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [bulk RNA]

Project description:Purpose: To identify the cell types that contribute to CFTR expression and function within the proximal-distal axis of the normal human lung. Methods: Single cell RNA-seq (scRNA-seq) was performed on freshly isolated human large and small airway epithelial cells. Single cell-based RNA in situ hybridization (scRNA-ISH) and quantitative RT-PCR (scqRT-PCR) were performed for validation. In vitro culture systems correlated CFTR function to cell types. Lentiviruses were used for cell-type specific transduction of wild-type CFTR in CF cells. Results: scRNA-seq identified secretory cells as dominating CFTR expression in normal human large and particularly small airways, followed by basal cells. Ionocytes expressed the highest CFTR levels but were rare, while expression in ciliated cells was infrequent and low. scRNA-ISH, and scqRT-PCR confirmed the scRNA-seq findings. CF lungs exhibited distributions of CFTR and ionocytes similar to normal controls. CFTR-mediated Cl- secretion tracked secretory cell, not ionocyte, densities. Further, the nucleotide-purinergic regulatory system that controls CFTR-mediated hydration was associated with secretory cells. Lentiviral transduction of wild-type CFTR produced CFTR-mediated Cl- secretion in CF airway secretory cells but not ciliated cells. Conclusions: Secretory cells dominate CFTR expression and function in human airway superficial epithelia. CFTR therapies may need to restore CFTR function to multiple cell types, with a focus on secretory cells.

2020-12-16 | GSE160674 | GEO

Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [single-cell RNA-seq]

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Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [bulk RNA]

Project description:Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [bulk RNA]

| PRJNA673906 | ENA

Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [single-cell RNA-seq]

Project description:Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia [single-cell RNA-seq]

| PRJNA673905 | ENA

Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia

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

2020-12-16 | GSE160675 | GEO

A microRNA network regulates expression and biosynthesis of CFTR and CFTR-M-NM-^TF508.

Project description:Production of functional proteins requires multiple steps including gene transcription and post-translational processing. MicroRNAs (miRNA) can regulate individual stages of these processes. Despite the importance of the cystic fibrosis transmembrane conductance regulator (CFTR) channel for epithelial anion transport, how its expression is regulated remains uncertain. We discovered that microRNA-138 regulates CFTR expression through its interactions with the transcriptional regulatory protein SIN3A. Treating airway epithelia with a miR-138 mimic increased CFTR mRNA and also enhanced CFTR abundance and transepithelial Cl- permeability independently of elevated mRNA levels. A miR-138 anti-miR had the opposite effects. Importantly, miR-138 altered the expression of many genes encoding proteins that associate with CFTR and may influence its biosynthesis. The most common CFTR mutation, M-NM-^TF508, causes protein misfolding, degradation, and cystic fibrosis. Remarkably, manipulating the miR-138 regulatory network also improved biosynthesis of CFTR-M-NM-^TF508 and restored Cl- transport to cystic fibrosis airway epithelia. This novel miRNA-regulated network directs gene expression from the chromosome to the cell membrane, indicating that an individual miRNA can control a cellular process broader than previously recognized. This discovery also provides new therapeutic avenues for restoring CFTR function to cells affected by the most common cystic fibrosis mutation. 12 samples of Calu-3 cells representing different interventions.

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A microRNA network regulates expression and biosynthesis of CFTR and CFTR-ΔF508.

Project description:Production of functional proteins requires multiple steps including gene transcription and post-translational processing. MicroRNAs (miRNA) can regulate individual stages of these processes. Despite the importance of the cystic fibrosis transmembrane conductance regulator (CFTR) channel for epithelial anion transport, how its expression is regulated remains uncertain. We discovered that microRNA-138 regulates CFTR expression through its interactions with the transcriptional regulatory protein SIN3A. Treating airway epithelia with a miR-138 mimic increased CFTR mRNA and also enhanced CFTR abundance and transepithelial Cl- permeability independently of elevated mRNA levels. A miR-138 anti-miR had the opposite effects. Importantly, miR-138 altered the expression of many genes encoding proteins that associate with CFTR and may influence its biosynthesis. The most common CFTR mutation, ΔF508, causes protein misfolding, degradation, and cystic fibrosis. Remarkably, manipulating the miR-138 regulatory network also improved biosynthesis of CFTR-ΔF508 and restored Cl- transport to cystic fibrosis airway epithelia. This novel miRNA-regulated network directs gene expression from the chromosome to the cell membrane, indicating that an individual miRNA can control a cellular process broader than previously recognized. This discovery also provides new therapeutic avenues for restoring CFTR function to cells affected by the most common cystic fibrosis mutation.

2012-09-04 | GSE38956 | GEO

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2023-03-02 | GSE203007 | GEO

CF (1565) vs CFTR-corrected (1564) iPSC-airway at ALI

Project description:Purpose of experiment :To 1) evaluate for the presence of pulmonary ionocytes, 2) investigate the role of the CFTR in airway epithelium. Description of samples: 1564 (CF-repaired), 1565 (CF DF508homozygous) iPSC-airway epithelium through basal cell intermediate. iPSC-D15CD47/CD26sort- NGFR sort x 2

2023-03-02 | GSE203008 | GEO

Expression data from human airway epithelia exposed to IL13

Project description:IL13 exposure results in a distinct gene expression profile in human airway epithelia. We investigated whether this expression profile can be used to identify compounds able to block goblet cell metaplasia We used microarrays to determine transcriptional changes in cultures of primary human airway epithelia grown at the air-liquid interface after exposure to 20 ng/mL recombinant human IL13

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