Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profile of alveolar macrophages (AM) from bleomycin treated mice.

ABSTRACT: Osteopontin (OPN, Spp1-/-) is considered detrimental in pulmonary fibrosis. However, effect of OPN produced by AMs during pulmonary fibrosis is not known. We used bulk RNA sequencing to analyze the effect of OPN in AMs from bleomycin treated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE202348 | GEO | 2024/03/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Bleomycin model of fibrosis and resolution phase in old and young mice

Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Young (3 months) and old (21 months) mice were treated with Bleomycin or with control saline solution and analyzed transcript and protein expression over 8 weeks (Day 0, 14, 21, 28, 35, 42, 49, 56).

2023-08-09 | PXD041050 | Pride

Bleomycin model of fibrosis and resolution phase in old and young mice

2024-09-10 | PXD040530 | Pride

Ablation or Inhibition of Protein Disulfide Isomerase A3 (PDIA3) in Aberrant Club Cells Attenuates Osteopontin (SPP1) Production and Pulmonary Fibrosis

Project description:Rationale: The role of club cells in the pathology of Idiopathic Pulmonary Fibrosis IPF is not well understood. PDIA3, an endoplasmic reticulum (ER) based redox chaperone catalyzes the cysteine disulfide bonds (-S-S-) in various fibrosis-related proteins; however, mechanisms of action of PDIA3 in pulmonary fibrosis is not fully elucidated. Objectives: To examine the role of club cells and PDIA3 in the pathogenesis of pulmonary fibrosis (PF) and therapeutic potential of inhibition of PDIA3 in PF. Methods: The impact of PDIA3 and aberrant club cells in PF was studied by retrospective analysis of human transcriptome data from LGRC, and specific deletion and inhibition of PDIA3 in club cells and blocking Osteopontin (SPP1) downstream of PDIA3 in mice. Measurements and Main Results: The PDIA3 along with club cell secretory protein (SCGB1A1 or CCSP) signatures are upregulated in IPF compared to control patients, and PDIA3 increases correlate with a decrease in lung function in IPF patients. The Bleomycin (BLM) model of PF showed increases in aberrant CCSP and PDIA3 positive cells in the lung parenchyma. Ablation of Pdia3, specifically in CCSP cells, decreases CCSP cells along with PF in mice. The therapeutic administration of a PDI inhibitor LOC14 reversed the BLM-induced CCSP cells and PF in mice. The proteomic screen of the PDIA3 partners revealed SPP1 as a major interactor in PF. Blocking SPP1 attenuated the development of PF in mice. Conclusions: Collectively, this study demonstrates a new relationship of club cells, with PDIA3, SPP1, and a putative pathological function of club cells in pulmonary fibrosis.

2021-11-11 | PXD021715 | Pride

Transcriptomic changes driving pulmonary fibrosis resolution in young and old Bleomycin-treated mice

Project description:Bleomycin-induced pulmonary fibrosis in mice mimics major hallmarks of idiopathic pulmonary fibrosis, yet in this model it spontaneously resolves over time. We studied molecular mechanisms of fibrosis resolution and lung repair, focusing on transcriptional and proteomic signatures and the effect of aging. Old mice showed delayed and incomplete lung function recovery 8 weeks after Bleomycin instillation. This shift in structural and functional repair in old Bleomycin-treated mice was reflected in a temporal shift in gene and protein expression. We reveal gene signatures and signaling pathways which underpin the lung repair process.

2023-10-16 | GSE218997 | GEO

Gene network analysis of interstitial macrophages after treatment with induced pluripotent stem cells secretome (iPSC-cm) in the bleomycin injured rat lung

Project description:Idiopathic pulmonary fibrosis (IPF) is a complex disease involving various cell types. Macrophages are essential in maintenance of physiological homeostasis, wound repair and fibrosis in the lung. Macrophages play a crucial role in repair and remodeling by altering their phenotype and secretory pattern in response to injury. The secretome of induced pluripotent stem cells (iPSC-cm) attenuates injury and fibrosis in bleomycin injured rat lungs. In the current study, we evaluate the effect of iPSC-cm on interstitial macrophage gene expression and phenotype in bleomycin injured rat lungs in vivo. Â iPSC-cm was intratracheally instilled 7 days after bleomycin induced lung injury and assessed 7 days later and single cell isolation was performed. Macrophages were FACS sorted and microarray analysis was performed. We characterized changes in the rat lung interstitial macrophages using transcriptional profiling.

2017-03-20 | E-MTAB-5619 | biostudies-arrayexpress

Proteomic profiling of young and old mice in the bleomycin model

Project description:The most preclinical used in vivo model to study lung fibrosis is the bleomycin-induced lung fibrosis model in 2-3-month-old mice. Although this model resembles key aspects of idiopathic pulmonary fibrosis (IPF), there are limitations in its predictability for the human disease. One of the main differences is the juvenile age of animals that are usually used in experiments, resembling humans of around 20 years. Because IPF patients are usually older than 60 years, aging appears to play an important role in the pathogenesis of lung fibrosis. We here compared young (3 months) and old (21 months) mice 21 days after intratracheal bleomycin instillation.

2024-09-10 | PXD026222 | Pride

Gene expression profiling of experimental-induced pulmonary fibrosis in subcutaneous bleomycin-treated mice vs EXT-treated mice

Project description:Analysis of whole genome gene expression levels in distal lung tissue from mice with systemically bleomycin-induced pulmonary fibrosis. The hypothesis is that bleomycin promotes a specific genotype associated with development of pulmonary fibrosis and that treatment with compound EXT reduces the induction of genes related to the early progression of fibrosis.

2017-09-06 | GSE103511 | GEO

A murine systemic bleomycin model of scleroderma

Project description:A well-characterized mouse model of SSc involves daily subcutaneous injections of the antitumor antibiotic bleomycin (BLM), which leads to localized dermal fibrosis as well as pulmonary fibrosis. We have termed this the “Systemic Bleomycin Model” to distinguish it from the already-established Intratracheal (IT) model. We utilize this model, which mimics several key features of human SSc, to examine the pathological mechanisms underlying the development and progression of fibrosis in SSc.

2019-06-18 | GSE132869 | GEO

Studies on bleomycin-induced lung fibrosis in mice

Project description:We perfomed a microRNA microarray on to assess differentially expressed miRNAs in bleomycin-induced lung fibrosis in mice. To induce pulmonary fibrosis, belomycine (Sigma-Aldrich, St Louis, MO) was dissolved and administred intratracheally at a dose of 1.5U/kg body weight. Control animals received saline only. 21 days post bleomycin treatment, mice were sacrificed and lung tissue were collected for RNA extraction and microRNA microarray.

2020-08-07 | GSE155823 | GEO

Gene expression analysis of bleomycin-challenged mouse lung tissues with/without repetitive hyperbaric oxygen treatment

Project description:Idiopathic pulmonary fibrosis (IPF) is a dreadful, chronic, and irreversibly progressive disease leading to death with few effective treatments. Our previous study suggested that repetitive hyperbaric oxygen (HBO) treatment alleviates bleomycin-induced pulmonary fibrosis in mice, but the underlying mechanism is not clear. In this study, we compared the RNA-seq data from bleomycin challenged mouse lung tissues with or without repetitive HBO treatment, to figure out the affected biological processes and pathways. Combined with integrative analysis of public data from GEO, our study support HBO treatment as a viable strategy against pulmonary fibrosis.

2022-09-29 | GSE200109 | 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