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Epithelial-derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation

ABSTRACT: Epithelial-derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation

PROVIDER: PRJNA827583 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18779920.fastq.gz	Fastqsanger.gz
	SRR18779921.fastq.gz	Fastqsanger.gz
	SRR18779922.fastq.gz	Fastqsanger.gz
	SRR18779923.fastq.gz	Fastqsanger.gz
	SRR18779924.fastq.gz	Fastqsanger.gz

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Epithelial-derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation

Project description:To explore the downstream mechanisms of Notch2 induced M2 macrophage polarization during mechanical ventilation, the BMDMs-treated with exosomes for non-cyclical-stretched or cyclical-stretced epithelial cells for 12 h were subjected to RNA-seq.

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Epithelial‑derived exosomes promote M2 macrophage polarization via Notch2/SOCS1 during mechanical ventilation.

Project description:Alveolar macrophages (AMs) play an essential role in ventilator‑induced lung injury (VILI). Exosomes and their cargo, including microRNAs (miRNAs/miRs) serve as regulators of the intercellular communications between macrophages and epithelial cells (ECs), and are involved in maintaining homeostasis in lung tissue. The present study found that exosomes released by ECs subjected to cyclic stretching promoted M2 macrophage polarization. It was demonstrated that miR‑21a‑5p, upregulated in epithelial‑derived exosomes, increased the percentage of M2 macrophages by suppressing the expression of Notch2 and the suppressor of cytokine signaling 1 (SOCS1). The overexpression of Notch2 decreased the percentage of M2 macrophages. However, these effects were reversed by the downregulation of SOCS1. The percentage of M2 macrophages was increased in both short‑term high‑ and low‑tidal‑volume mechanical ventilation, and the administration of exosomes‑derived from cyclically stretched ECs had the same function. However, the administration of miR‑21a‑5p antagomir decreased M2 macrophage activation induced by cyclically stretched ECs or ventilation. Thus, the present study demonstrates that the intercellular transferring of exosomes from ECs to AMs promotes M2 macrophage polarization. Exosomes may prove to be a novel treatment for VILI.

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Effect of mechanical ventilation and mechanical ventilationon with positive end expiratory pressure(PEEP) application on diaphragmatic dysfunction in rabbits

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Project description:Acute respiratory distress syndrome (ARDS) results in significant morbidity and mortality, especially in the elderly. Mechanical ventilation, a common supportive treatment for ARDS, is necessary for maintaining gas exchange, but can also propagate injury. We hypothesized that aging would exacerbate the pathophysiological responses to mechanical ventilation. Young and aged male mice were mechanically ventilated and changes in surfactant function, inflammation, and vascular permeability were assessed. Additionally, single-cell RNA sequencing was used to delineate cell-specific transcriptional changes. The results showed that surfactant dysfunction was augmented in aged mice, while inflammation was less pronounced in aged animals. Futhermore, vascular permeability was significantly increased with aging. Differential gene expression and pathway analyses revealed that aged endothelial cells exhibited altered cell-cell junction formation and that alveolar macrophages in aged mice showed a blunted inflammatory response. These results highlight the complex interplay between aging and mechanical ventilation, including an age-related predisposition to endothelial barrier dysfunction due to altered cell-cell junction formation and decreased inflammation, potentially due to immune exhaustion. It is concluded that age-related vascular changes may underlie the increased susceptibility to injury during mechanical ventilation in elderly patients.

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Age Dependent Gene Expression Responses to Inhaled Lipopolysaccharide Combined with Mechanical Ventilation

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Single-nucleus transcriptomic profiling of the diaphragm during mechanical ventilation

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MAP Kinase Phosphatase-1 Modulates Regional Effects of Injurious Mechanical Ventilation in Rodent Lungs

Project description:Scientific knowledge on the subjects: Injurious mechanical ventilation amplifies acute lung injury in a heterogeneous and regional fashion but the molecular mechanisms underlying regional lung injury and the protective effects of prone positioning are unclear. Regionally injurious ventilation is associated with discrete differential lung transcriptomic changes. Ventilating in the prone, compared with the supine position abrogates regional injury by depressing MKP-1.

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