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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

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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

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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]

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

Project description: Not available

| S-EPMC8021117 | biostudies-literature

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

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.

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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

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

Project description: Not available

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

2012-12-04 | GSE37693 | GEO

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

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