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Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk [miRNA-Seq]

ABSTRACT: Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk [miRNA-Seq]

PROVIDER: PRJNA658361 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12486391.fastq.gz	Fastqsanger.gz
	SRR12486392.fastq.gz	Fastqsanger.gz
	SRR12486393.fastq.gz	Fastqsanger.gz
	SRR12486394.fastq.gz	Fastqsanger.gz

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Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk

Project description:Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk

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Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk [RNA-Seq]

Project description:Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk [RNA-Seq]

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Human bronchial epithelial cell-derived extracellular vesicles attenuate pulmonary fibrosis through inhibiting TGF-β-WNT crosstalk [RNA-Seq]

Project description:Idiopathic pulmonary fibrosis (IPF) is characterized by devastating and progressive lung parenchymal ﬁbrosis with poor prognosis. An aberrant recapitulation of lung developmental genes including transforming growth factor (TGF)-β and WNT has been widely implicated in the abnormal wound healing process following repetitive alveolar epithelial injury during IPF pathogenesis. Extracellular vesicles (EVs) including exosomes and microvesicles have been shown to carry various bioactive molecules and are involved in a variety of physiological and pathological processes. Here, we demonstrate that human bronchial epithelial cell-derived EVs (HBEC EVs) inhibited TGF-β-induced both myofibroblast differentiation and lung epithelial cellular senescence through attenuating WNT signaling. To ask how HBEC-EVs inhibited TGF-β-induced both myofibroblast differentiation and lung epithelial cellular senescence through attenuating WNT signaling, miRNA RNA-seq of HBEC-EVs was performed.

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Project description:Idiopathic pulmonary fibrosis (IPF) is characterized by devastating and progressive lung parenchymal fibrosis, resulting in poor patient prognosis. An aberrant recapitulation of developmental lung gene expression, including genes for transforming growth factor (TGF)-β and WNT, has been widely implicated in the pathogenic IPF wound healing process that results from repetitive alveolar epithelial injury. Extracellular vesicles (EVs) have been shown to carry bioactive molecules and to be involved in various physiological and pathological processes. Here, we demonstrate that, by attenuating WNT signalling, human bronchial epithelial cell-derived EVs (HBEC EVs) inhibit TGF-β mediated induction of both myofibroblast differentiation and lung epithelial cellular senescence. This effect of HBEC EVs is more pronounced than that observed with mesenchymal stem cell-derived EVs. Mechanistically, the HBEC EV microRNA (miRNA) cargo is primarily responsible for attenuating both myofibroblast differentiation and cellular senescence. This attenuation occurs via inhibition of canonical and non-canonical WNT signalling pathways. Among enriched miRNA species present in HBEC EVs, miR-16, miR-26a, miR-26b, miR-141, miR-148a, and miR-200a are mechanistically involved in reducing WNT5A and WNT10B expression in LFs, and in reducing WNT3A, WNT5A, and WNT10B expression in HBECs. Mouse models utilizing intratracheal administration of EVs demonstrate efficient attenuation of bleomycin-induced lung fibrosis development accompanied by reduced expression of both β-catenin and markers of cellular senescence. These findings indicate that EVs derived from normal resident lung HBECs may possess anti-fibrotic properties. They further suggest that, via miRNA-mediated inhibition of TGF-β-WNT crosstalk, HBEC EVs administration can be a promising anti-fibrotic modality of treatment for IPF.

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