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Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

ABSTRACT: Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

PROVIDER: PRJNA933176 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23384980.fastq.gz	Fastqsanger.gz
	SRR23384981.fastq.gz	Fastqsanger.gz
	SRR23384982.fastq.gz	Fastqsanger.gz
	SRR23384983.fastq.gz	Fastqsanger.gz
	SRR23384984.fastq.gz	Fastqsanger.gz

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Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection.

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Maladaptive TGF-β Signals to the Alveolar Epithelium Drive Fibrosis after COVID-19 Infection

Project description:We have performed single cell RNA sequencing on explant tissue of post-acute sequelae SARS-CoV-2 infection (PASC) patients. The study focused on epithelial cells (Epcam+) and immune cells (CD45+) cells. We further compared our PASC sample with Donor and IPF samples from GSE146981 and GSE135893.

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Quantitative Proteomic Analysis in Alveolar Type II Cells Reveals the Different Capacities of RAS and TGF-β to Induce Epithelial–Mesenchymal Transition

Project description:Alveolar type II (ATII) epithelial cells function as stem cells, contributing to alveolar renewal, repair and cancer. Therefore, they are a highly relevant model for studying lung diseases, including acute injury, fibrosis and cancer, in which signals transduced by RAS and transforming growth factor (TGF)-ß play critical roles. To identify downstream molecular events following RAS and/or TGF-ß activation, we performed proteomic analysis using a quantitative label-free approach (LC-HDMSE) to provide in-depth proteome coverage and estimates of protein concentration in absolute amounts. Contact: pjss@soton.ac.uk

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Maladaptive functional changes in alveolar fibroblasts due to perinatal hyperoxia impair epithelial differentiation

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Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.

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