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IPF Cell Atlas

ABSTRACT: IPF Cell Atlas

PROVIDER: PRJNA563828 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR21407800_1.fastq.gz	Fastqsanger.gz
	SRR21407800_2.fastq.gz	Fastqsanger.gz
	SRR21407801_1.fastq.gz	Fastqsanger.gz
	SRR21407801_2.fastq.gz	Fastqsanger.gz
	SRR21407802_1.fastq.gz	Fastqsanger.gz

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Project description:Accelerated senescence in lung epithelial cells is known to play a key role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the exact mechanisms underlying the IPF-related epithelial cell phenotype have yet to be elucidated. Increasing evidence supports the concept that extracellular vesicles (EVs), including exosomes and microvesicles, mediate intercellular communication that contributes to diverse aspects of physiology and pathogenesis. Here, we demonstrate that lung fibroblasts (LFs) from IPF patients accelerate epithelial cell senescence via EV-mediated transfer of LF-derived pathogenic cargo to lung epithelial cells. Mechanistically, IPF LF-derived EVs increase mitochondrial reactive oxygen species (mtROS) and associated mitochondrial damage in lung epithelial cells, leading to mtROS-mediated activation of the DNA damage response and subsequent epithelial cell senescence. We show that IPF LF-derived EVs contain elevated levels of miR-23b-3p and miR-494-3p that are responsible for suppressing SIRT3, resulting in the EV-induced phenotypic changes of lung epithelial cells. Furthermore, we observe that miR-23b-3p and miR-494-3p expression increases in lung epithelial cells from IPF patients’ lungs. Finally, the levels of miR-23b-3p and 494-3p found in IPF LF-derived EVs correlate positively with IPF disease severity. These findings reveal that the accelerated epithelial cell mitochondrial damage and senescence observed during IPF pathogenesis are caused by a novel mechanism in which SIRT3 is suppressed by miR-containing EVs derived from IPF fibroblasts.

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Project description:Idiopathic pulmonary fibrosis (IPF) is a disease related to AT2 cell. We used flow cytometry to analyze the epithelial component of donor and IPF lungs. From the live cells, we first excluded the CD31PosCD45Pos and then selected the EPCAMPos cells for further analysis using the human AT2 cell marker HTll-280 and the surface marker PD-L1. Our data indicate that, the bona fide differentiated AT2 cells (HTll-280High PD-L1Neg), were drastically reduced in the context of IPF. More interestingly, the number of HTll-280Low/Neg PD-L1High was drastically increased, suggesting that HTll-280Low PD-L1High epithelial cells could represent a pool of progenitors linked to the deficient AT2 lineage. The aim of this experiment is further characterization of AT2 and PDL1+ cells in donor and IPF.

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IPF versus Control

Project description:Archived lung tissues of patients with IPF were obtained from the tissue bank of the Department of Pathology at the University of Pittsburgh. The diagnosis of IPF was confirmed by open lung biopsy. All patients fulfilled the criteria of the American Thoracic Society and European Respiratory Society for the diagnosis of IPF. Normal histology lung tissues resected from patients with lung cancer were used as controls. Keywords: parallel sample

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