Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epithelial miR-141 regulates IL-13-induced airway mucus production [single-cell RNA-seq]

ABSTRACT: Epithelial miR-141 regulates IL-13-induced airway mucus production [single-cell RNA-seq]

PROVIDER: PRJNA688515 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13324946.fastq.gz	Fastqsanger.gz
	SRR13324947.fastq.gz	Fastqsanger.gz
	SRR13324948.fastq.gz	Fastqsanger.gz
	SRR13324949.fastq.gz	Fastqsanger.gz
	SRR13324950.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Epithelial miR-141 regulates IL-13-induced airway mucus production

Project description:We performed RNA sequencing of gene expression in primary human bronchial epithelial cells that have undergone CRISPR/Cas9-based targeting of MIR141. The goal was to identify the role of miR-141 in goblet cell mucus production. CRISPR-targeted cells were differentiated at air-liquid-interface and stimulated with IL-13 to induce goblet cell hyperplasia.

2020-12-05 | GSE162696 | GEO

Epithelial miR-141 regulates IL-13-induced airway mucus production

Project description:Epithelial miR-141 regulates IL-13-induced airway mucus production

| PRJNA682625 | ENA

Epithelial miR-141 regulates IL-13-induced airway mucus production [miRNA-seq]

Project description:Epithelial miR-141 regulates IL-13-induced airway mucus production [miRNA-seq]

| PRJNA688922 | ENA

Epithelial miR-141 regulates IL-13-induced airway mucus production.

Project description:IL-13-induced goblet cell metaplasia contributes to airway remodeling and pathological mucus hypersecretion in asthma. miRNAs are potent modulators of cellular responses, but their role in mucus regulation is largely unexplored. We hypothesized that airway epithelial miRNAs play roles in IL-13-induced mucus regulation. miR-141 is highly expressed in human and mouse airway epithelium, is altered in bronchial brushings from asthmatic subjects at baseline, and is induced shortly after airway allergen exposure. We established a CRISPR/Cas9-based protocol to target miR-141 in primary human bronchial epithelial cells that were differentiated at air-liquid-interface, and goblet cell hyperplasia was induced by IL-13 stimulation. miR-141 disruption resulted in decreased goblet cell frequency, intracellular MUC5AC, and total secreted mucus. These effects correlated with a reduction in a goblet cell gene expression signature and enrichment of a basal cell gene expression signature defined by single cell RNA sequencing. Furthermore, intranasal administration of a sequence-specific mmu-miR-141-3p inhibitor in mice decreased Aspergillus-induced secreted mucus and mucus-producing cells in the lung and reduced airway hyperresponsiveness without affecting cellular inflammation. In conclusion, we have identified a miRNA that regulates pathological airway mucus production and is amenable to therapeutic manipulation through an inhaled route.

| S-EPMC8021117 | biostudies-literature

Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

Project description:Primary culture airway epithelial cells, grown under physiologic air-liquid interface conditions, with, or without IL-13 in order to study the effects of this cytokine on mucous cell metaplasia, an important feature of asthma and COPD. Keywords: IL13, mucus, goblet cell RNA was isolated from primary culture airway epithelial cells grown at air-liquid interface, treated with or without IL-13 for 21 days.

2012-12-04 | E-GEOD-37693 | biostudies-arrayexpress

Epithelial miR-141 regulates IL-13-induced airway mucus production [miRNA-seq]

Project description:We performed small RNA sequencing (TruSeq) of gene expression on bronchial cells from human bronchial epithelial brushings from 16 independent subjects whose samples were classified as either healthy controls (with no asthma or lung disease) or steroid-naive asthmatics (subjects with asthma not using inhaled corticosteroids (ICS) for 6 weeks before enrollment that were studied at baseline ('Steroid-naive asthma - Baseline') or after 8 weeks of treatment with budesonide, 200 μg twice a day, ('Steroid-naive asthma - Post-ICS treatment')). The goal was to assess abundance of miRNAs in all the samples collectively.

2021-01-01 | GSE164119 | GEO

Gene Expression Effects of IL-13 on Primary Human Airway Epithelial Cells

2012-12-04 | GSE37693 | GEO

Epithelial miR-141 regulates IL-13-induced airway mucus production [single-cell RNA-seq]

Project description:We performed single cell RNA sequencing on bronchial cells from human bronchoalveolar lavage fluid from 4 independent study participants who had asthma and who underwent lung segmental allergen challenge with diluent or allergen (either house duse mite or cat). The goal was to assess total mRNAs in single cell preparations of bronchoalveolar lavage cells.

2020-12-30 | GSE164015 | GEO

IL-13-induced airway mucus production is attenuated by MAPK13 inhibition.

Project description:Increased mucus production is a common cause of morbidity and mortality in inflammatory airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis. However, the precise molecular mechanisms for pathogenic mucus production are largely undetermined. Accordingly, there are no specific and effective anti-mucus therapeutics. Here, we define a signaling pathway from chloride channel calcium-activated 1 (CLCA1) to MAPK13 that is responsible for IL-13-driven mucus production in human airway epithelial cells. The same pathway was also highly activated in the lungs of humans with excess mucus production due to COPD. We further validated the pathway by using structure-based drug design to develop a series of novel MAPK13 inhibitors with nanomolar potency that effectively reduced mucus production in human airway epithelial cells. These results uncover and validate a new pathway for regulating mucus production as well as a corresponding therapeutic approach to mucus overproduction in inflammatory airway diseases.

| S-EPMC3533556 | biostudies-literature

A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma

Project description:By incompletely understood mechanisms, type 2 (T2) inflammation present in the airways of severe asthmatics drives the formation of pathologic mucus which leads to airway mucus plugging. Here we investigate the molecular role and clinical significance of intelectin-1 (ITLN-1) in the development of pathologic airway mucus in asthma. Through analyses of human airway epithelial cells we find that ITLN1 gene expression is highly induced by interleukin-13 (IL-13) in a subset of metaplastic MUC5AC+ mucus secretory cells, and that ITLN-1 protein is a secreted component of IL-13-induced mucus. Additionally, we find ITLN-1 protein binds the C-terminus of the MUC5AC mucin and that its deletion in airway epithelial cells partially reverses IL-13-induced mucostasis. Through analysis of nasal airway epithelial brushings, we find that ITLN1 is highly expressed in T2-high asthmatics, when compared to T2-low children. Furthermore, we demonstrate that ITLN1 gene expression is significantly reduced and ITLN-1 protein expression is lost through a common genetic variant that is associated with protection from the formation of mucus plugs in T2-high asthma. This work identifies one of the first biomarkers and targetable pathways for the treatment of mucus obstruction in asthma.

2024-04-04 | GSE254127 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data