Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Histone modifications in lung epithelial cells

ABSTRACT: We report histone modifications in alveolar epithelial type 2 cells in homeostatic mice as well as CTGF-positive alveolar eptihelial cells in mice treated with Bleomycin.

ORGANISM(S): Mus musculus

PROVIDER: GSE141635 | GEO | 2020/06/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Histone modifications in lung epithelial cells

Project description:Histone modifications in lung epithelial cells

| PRJNA594274 | ENA

Multiple bleomycin exposed mouse lung epithelial type 2 cells

Project description:We analyze the mRNA level in multiple PBS or bleomycin exposed mouse lung alveolar epithelial type 2 cells

2021-02-09 | GSE110479 | GEO

Fgf10-Fgfr2b signaling generates basal cells and drives alveolar epithelial regeneration by bronchial epithelial stem cells after lung injury

Project description:Idiopathic pulmonary fibrosis (IPF) is a common form of interstitial lung disease (ILD) resulting in alveolar remodeling and progressive loss of pulmonary function due to chronic alveolar injury and failure to regenerate the respiratory epithelium. Histologically, fibrotic lesions and honeycomb structures expressing atypical proximal airway epithelial markers replace alveolar structures, the latter normally lined by alveolar type 1 (AT1) and AT2 cells. Bronchial epithelial stem cells (BESCs) can give rise to AT2 and AT1 cells or honeycomb cysts following bleomycin-mediated lung injury. However, little is known about what controls this binary decision or whether this decision can be reversed. Here we report that inactivation of Fgfr2b in BESCs impairs their contribution to both alveolar epithelial regeneration and honeycomb cysts after bleomycin injury. By contrast overexpression of Fgf10 in BESCs enhances fibrosis resolution by favoring the more desirable outcome of alveolar epithelial regeneration over the development of pathologic honeycomb cysts.

2019-03-30 | GSE129079 | GEO

Gene expression profiling on alveolar epithelial cells from mice intratracheally instilled with or without bleomycin or LPS.

Project description:We applied next-generation sequencing to investigate the gene expression profiles in mouse alveolar epithelial cells (AECs). We identified a number of differentially regulated genes in the AECs of mice with bleomycin induced pulmonary fibrosis and LPS induced acute lung injury.

2018-02-01 | GSE109913 | GEO

Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury

Project description:A hallmark of idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases is dysregulated repair of the alveolar epithelium. The Hippo pathway effector transcription factors YAP and TAZ are implicated as essential for type 1 and type 2 alveolar epithelial cell (AT1 and AT2) differentiation in the developing lung, yet aberrant activation of YAP/TAZ is a prominent feature of the dysregulated alveolar epithelium in IPF. In these studies, we sought to define the functional role of YAP/TAZ activity during alveolar regeneration. We demonstrated that Yap and Taz are normally activated in AT2 cells shortly after injury, and deletion of Yap/Taz in AT2 cells led to pathologic alveolar remodeling, failure of AT2 to AT1 cell differentiation, increased collagen deposition, exaggerated neutrophilic inflammation, and increased mortality following injury induced by a single dose of bleomycin. Loss of Yap/Taz activity prior to a LPS injury prevented AT1 cell regeneration, led to intra-alveolar collagen deposition, and resulted in persistent innate inflammation. Together these findings established that AT2 cell Yap/Taz activity is essential for functional alveolar epithelial repair and prevention of fibrotic remodeling.

2023-11-15 | GSE243135 | GEO

Expression data from lung mesenchymal cells in bleomycin-induced lung injury

Project description:Bleomycin-induced acute lung injury is characterized by mesenchymal cell activation, which leads to pulmonary fibrosis. They also have the potential to increase epithelial cells to regenerate alveolar epithelial cell integrity. We used microarrays to detail the change of global gene expression in lung mesenchymal cells in this process.

2022-09-15 | GSE208444 | GEO

Mouse feeder-free alveolar organoids treated by bleomycin

Project description:To investigate the direct effect of bleomycin on alveolar epithelium, feeder-free mouse alveolar organoids were treated by bleomycin (100μM) for 48 hours in vitro and then analyzed.

2022-08-21 | GSE211531 | GEO

Syndecan-1 promotes lung fibrosis by regulating epithelial reprogramming through extracellular vesicles (miRNA-Seq)

Project description:We studied transcriptomic changes of extracellular vesicles (EVs) in bronchoalveolar lavage fluid of bleomycin-injured wild-type and syndecan-1 deficient mice

2019-07-27 | GSE134948 | GEO

Depletion of club cells attenuates bleomycin-induced lung injury and fibrosis in mice

Project description:Background and objective: The role of bronchiolar epithelial cells in the pathogenesis of pulmonary fibrosis has not been addressed. We previously demonstrated that DNA damage was found in bronchiole at early phase, and subsequently extended to alveolar cells at later phase in bleomycin-induced pulmonary fibrosis in mice. Club cells are progenitor cells for bronchiole, and are recognized to play protective roles against lung inflammation and damage. The aim of the study was to elucidate the role of club cells in the development of pulmonary fibrosis. Methods: C57BL/6J mice were received naphthalene intraperitoneally at day -2 to deplete club cells, and were given intratracheal bleomycin or vehicle at day 0. Lung tissues were obtained at day 1, 7, and 14, and bronchoalveolar lavage was performed at day 14. Gene expression was analysed from bronchiolar ephithelial cells sampled by laser captured microdissection at day 14. Results: Surprisingly, naphthalene-induced club cell depletion protected mice from bleomycin-induced lung injury and fibrosis. We conclude that club cells are involved in the development of lung injury and fibrosis.

2017-02-08 | GSE94522 | GEO

Time makes histone H3 modifications drift

Project description:To disclose the epigenetic drift of time passing, we determined the genome-wide distributions of mono- and tri-methylated lysine 4 and acetylated and tri-methylated lysine 27 of histone H3 in the livers of healthy 3, 6 and 12 months old C57BL/6 mice. The comparison of different age profiles of histone H3 marks revealed global redistribution of histone H3 modifications with time, in particular in intergenic regions and near transcription start sites, as well as altered correlation between the profiles of different histone modifications. Moreover, feeding mice with caloric restriction diet, a treatment known to retard aging, preserved younger state of histone H3 in these genomic regions.

2022-07-13 | GSE179090 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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