Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Interrupted reprogramming of Alveolar Type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis

ABSTRACT: Interrupted reprogramming of Alveolar Type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis

PROVIDER: PRJNA474235 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Interrupted reprogramming of Alveolar Type II cells induces progenitor-like cells that ameliorate pulmonary fibrosis

Project description:We describe here an interrupted reprogramming strategy to generate "induced Progenitor-Like (iPL) cells" from Alveolar Epithelial Type II (AEC-II) cells. A carefully defined period of transient expression of reprogramming factors (Oct4, Sox2, Klf4 and c-Myc; OSKM) is able to rescue the limited in vitro clonogenic capacity of AEC-II cells, potentially by activation of a bipotential progenitor-like state. Microarray analysis of genome-wide transcriptional changes showed the ability of AEC-II-iPL cells to return to the original phenotype

2018-09-26 | GSE115247 | GEO

Resetting proteostasis in aged animals with ISRIB prevents recruitment of profibrotic monocyte-derived alveolar macrophages during pulmonary fibrosis

Project description:Aging is among the most important risk factors for the development of pulmonary fibrosis. Inappropriate or prolonged activation of the integrated stress response has been implicated in the pathobiology of both aging and pulmonary fibrosis. We found that a small molecule that relieves translational inhibition induced by activation of the integrated stress response (ISRIB) attenuated the severity pulmonary fibrosis in young and old mice. We demonstrate that severe fibrosis in old mice was associated with increased number of pathogenic monocyte-derived alveolar macrophages. Using transcriptomic profiling we found that ISRIB modulates stress response signaling in alveolar epithelial cells resulting in decreased recruitment of pathogenic monocyte-derived alveolar macrophages. Thus our data suggest that inhibition of the integrated stress response in the lung epithelium can ameliorate pulmonary fibrosis by preventing the recruitment of monocyte-derived alveolar macrophages.

2021-04-16 | GSE145295 | GEO

Resetting proteostasis in aged animals with ISRIB prevents recruitment of profibrotic monocyte-derived alveolar macrophages during pulmonary fibrosis [AT2]

2021-04-16 | GSE145771 | GEO

Resetting proteostasis in aged animals with ISRIB prevents recruitment of profibrotic monocyte-derived alveolar macrophages during pulmonary fibrosis [dataset 2]

2021-04-16 | GSE145590 | GEO

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (SPC+ cells)

Project description:We developed an in vitro model of pulmonary fibrosis using alveolar organoids, consisting of human induced pluripotent stem cell-derived alveolar epithelial cells and human lung fibroblasts. In this model, fibroblasts were activated by bleomysin (BLM) treatment in an epithelial cell-dependent manner simillar to the pathogenic mechanism observed in pulmonary fibrosis.

2021-11-19 | GSE172122 | GEO

Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis

Project description:Pulmonary alveolar microlithiasis is an autosomal recessive lung disease caused by a deficiency in the pulmonary epithelial Npt2b sodium-phosphate co-transporter that results in accumulation of phosphate and formation of hydroxyapatite microliths in the alveolar space. The single cell transcriptomic analysis of a pulmonary alveolar microlithiasis lung explant showing a robust osteoclast gene signature in alveolar monocytes and the finding that calcium phosphate microliths contain a rich protein and lipid matrix that includes bone resorbing osteoclast enzymes and other proteins suggested a role for osteoclast-like cells in the host response to microliths. While investigating the mechanisms of microlith clearance, we found that Npt2b modulates pulmonary phosphate homeostasis through effects on alternative phosphate transporter activity and alveolar osteoprotegerin, and that microliths induce osteoclast formation and activation in a receptor activator of nuclear factor kappa B (NF-kB) ligand and dietary phosphate dependent manner. This work reveals that Npt2b and pulmonary osteoclast like cells play key roles in pulmonary homeostasis and suggest potential new therapeutic targets for the treatment of lung disease.

2023-02-16 | MSV000091302 | MassIVE

Disease modeling of pulmonary fibrosis using human iPS cell-derived alveolar organoids (fibroblasts)

2021-11-19 | GSE172121 | GEO

GNPS - Insights into pulmonary phosphate homeostasis and osteoclastogenesis emerge from the study of pulmonary alveolar microlithiasis

2023-02-16 | MSV000091302 | GNPS

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

Genetic Recording of Transient Endothelial Activation in Distinct Alveolar Capillary Cells during Pulmonary Fibrosis

Project description:Endothelial to mesenchymal transition (EndoMT) is essential for embryonic development. However, the contribution of ECs to fibroblasts through EndoMT remains highly controversial in adult pathological conditions. Here, our dual-recombinase genetic system precisely captured extensive mesenchymal gene activation events of alveolar capillary cells in chronic TAC-induced pulmonary hypertension and fibrosis. Moreover, this type of endothelial activation was specifically observed in Plvap+ gCap, but not CAR4+ aCap capillary cells. In addition, our genetic tool confirmed the contribution of resident fibroblasts to pulmonary fibrosis. Unraveling the process of endothelial activation provides novel insights into potential therapeutic strategies targeting heart failure-induced pulmonary fibrosis.

2024-09-18 | GSE277471 | 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