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

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

PROVIDER: PRJNA688922 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13338271.fastq.gz	Fastqsanger.gz
	SRR13338272.fastq.gz	Fastqsanger.gz
	SRR13338273.fastq.gz	Fastqsanger.gz
	SRR13338274.fastq.gz	Fastqsanger.gz
	SRR13338275.fastq.gz	Fastqsanger.gz

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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.

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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.

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.

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

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

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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.

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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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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.

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