Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cell competition drives bronchiolization and pulmonary fibrosis

ABSTRACT: Cell competition drives bronchiolization and pulmonary fibrosis

PROVIDER: PRJNA1186651 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31362105.fastq.gz	Fastqsanger.gz
	SRR31362106.fastq.gz	Fastqsanger.gz
	SRR31362107.fastq.gz	Fastqsanger.gz
	SRR31362108.fastq.gz	Fastqsanger.gz
	SRR31362109.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

Cell competition drives bronchiolization and pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive respiratory scarring disease arising from the maladaptive differentiation of lung stem cells into bronchial epithelial cells rather than into alveolar type 1 (AT1) cells, which are responsible for gas exchange. Here, we report that healthy lungs maintain their stem cells through tonic Hippo and β-catenin signaling, which promote Yap/Taz degradation and allow for low level expression of the Wnt target gene Myc. Inactivation of upstream activators of the Hippo pathway in lung stem cells inhibits this tonic β-catenin signaling and Myc expression and promotes their Taz-mediated differentiation into AT1 cells. Vice versa, increased Myc in collaboration with Yap promotes the differentiation of lung stem cells along the basal and myoepithelial like lineages allowing them to invade and bronchiolize the lung parenchyma in a process reminiscent of submucosal gland development. Our findings indicate that stem cells exhibiting the highest Myc levels become supercompetitors that drive remodeling, whereas loser cells with lower Myc levels terminally differentiate into AT1 cells

2024-11-27 | GSE282002 | GEO

Single Cell Analysis of Pulmonary Fibrosis

Project description:Single Cell Analysis of Pulmonary Fibrosis

| PRJNA507827 | ENA

Single Cell Analysis of Pulmonary Fibrosis

Project description:Single Cell Analysis of Pulmonary Fibrosis

| PRJNA507826 | ENA

Dysfunctional ERG signaling drives pulmonary vascular aging and persistent fibrosis

Project description:Dysfunctional ERG signaling drives pulmonary vascular aging and persistent fibrosis

| PRJNA777445 | ENA

Single Cell Analysis of Pulmonary Fibrosis

Project description:<p>Pulmonary fibrosis is a heterogenous syndrome in which fibrotic scar replaces normal lung tissue. We performed massively parallel single-cell RNA-Seq on lung tissue from eight lung transplant donors and eight patients with pulmonary fibrosis. Combined with in situ RNA hybridization, with amplification, these data provide a molecular atlas of disease pathobiology. We identified a distinct, novel population of profibrotic alveolar macrophages exclusively in patients with fibrosis. Within epithelial cells, the expression of genes involved in Wnt secretion and response was restricted to non-overlapping cells. We identified rare cell populations including airway stem cells and senescent cells emerging during pulmonary fibrosis. Analysis of a cryobiopsy specimen from a patient with early disease supports the clinical application of single-cell RNA-Seq to develop personalized approaches to therapy.</p>

| phs001750 | dbGaP

Targeted immunotherapy rescues pulmonary fibrosis by against activated fibroblasts and regulating alveolar cell profile

Project description:Idiopathic pulmonary fibrosis (IPF) is a severe lung disease in the world, but has limited clinical therapies. Fibrosis maintains dynamic balance with overactivated fibroblasts. Given pulmonary cell regeneration, the lung may have self-repairing ability if fibrosis is removed by clearance of overactivated fibroblasts. The aim of the study is to evaluate therapeutic activity of transient CAR-T cells generated via a novelly designed LNP-mRNA system and address the relevant mechanism to epithelial cell polarization in a mouse model of bleomycin-induced IPF. Studies on proteomes and histology showed that fibrosis-induced ECM stiffening impaired epithelial cell polarization that limited cell’s self-healing ability. The proposed LNP-mRNA therapy eliminated overactivated fibroblasts and removed pulmonary fibrosis successfully. The decreased ECM stiffness and the improvement of extracellular environment facilitated re-establishment of cell polarity and restored the self-repairing ability of epithelial cell. Hence, LNP-mRNA treatment for IPF can recover pulmonary structure and function close to a healthy lung. This therapy shows a potential treatment for IPF patients.

2025-03-19 | PXD053333 | Pride

Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis (human)

Project description:Idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease associated with progressive scarring of lung tissue and declining pulmonary function in aging individuals. Here we employ data mining and single cell RNA sequencing (scRNAseq) to define candidate drivers of AT2 senescence in IPF lung tissue. We show that AT2 cells isolated from IPF lung tissue exhibit characteristic features of cellular senescence and reduced abundance of Sin3a, critical determinant of endodermal progenitor cell maintenance in the developing lung. Conditional loss of Sin3a within AT2 cells of the adult mouse lung activated a program of p53-dependent cellular senescence and AT2 cell depletion, leading to progressive pulmonary fibrosis. In contrast, ablation of AT2 cells through conditional activation of a DTA toxin gene led to transient fibrosis that resolved over time, suggesting that senescence of AT2 cells was a critical driver of progressive fibrosis. Activation of b6 integrin was observed within a subset of AT2 cells with Sin3a loss-of-function that localized to the advancing margin of advancing fibroproliferative lesions. Systemic inhibition of TGF signaling or delivery of senolytic drugs prevented lung fibrosis in Sin3a loss-of-function mice. Our findings establish a novel mouse model that recapitulates key pathological features of human IPA and show that p53-dependent senescence is a proximal regulator of TGF induction and progressive pulmonary fibrosis.

2020-06-30 | GSE132914 | GEO

Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis

Project description:Senescence rather than apoptosis of alveolar progenitor cells drives pulmonary fibrosis

| PRJNA549450 | ENA

Idiopathic pulmonary fibrosis (IPF)

Project description:Idiopathic pulmonary fibrosis (IPF)

| PRJNA802122 | ENA

Immune Checkpoint Regulation of Pulmonary Fibrosis [bulk RNA-seq]

Project description:Fibroblasts from idiopathic pulmonary fibrosis (IPF) patients acquire an invasive phenotype that is essential for progressive fibrosis. The immune checkpoint ligand CD274 (PD-L1) is up-regulated on invasive lung fibroblasts, regulated by P53 and FAK signaling, and drives lung fibrosis in a humanized IPF model in mice. Targeting CD274high fibroblasts blunted invasion in vitro and attenuated fibrosis in vivo, suggesting that CD274 may be a novel therapeutic target in IPF.

2019-05-17 | GSE118933 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data