Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of stimulated murine primary lung fibroblasts

ABSTRACT: Pulmonary fibrosis (PF) is both an independent disease and a pathologic basis for fibroproliferative lung diseases. Understanding of underlying mechanisms of PF is critical for developing effective therapeutics. Fibroblasts activation and extracellular matrix deposition are critical in pathogenesis of PF. Stimulation of certain factors can induce profibrotic changes in fibroblasts. Evaluation of associated genes in treated fibroblasts is helpfu to analyze the profibrotic changes of this critical effector cell for PF. We used microarrays to detail the global programme of gene expression following TGFβ and CCL1 stimulation of primary lung fibroblasts.

ORGANISM(S): Mus musculus

PROVIDER: GSE156314 | GEO | 2021/09/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

MiR-199a-5p determines fibroblast activation and pulmonary fibrogenesis

Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal pulmonary disorder characterized by fibroblast proliferation and the excess deposit of extracellular matrix proteins. The etiology of IPF is unknown, but a central role for microRNAs (miRNAs), a class of small non-coding regulatory RNAs, has been recently suggested. We report the upregulation of miR-199a-5p in mouse lungs undergoing bleomycin-induced fibrosis and also in human biopsies from IPF patients. Levels of miR-199a-5p were increased selectively in myofibroblasts and putative profibrotic effects of miR-199a-5p were further investigated in cultured lung fibroblasts. MiR-199a-5p expression was induced upon TGFβ exposure and ectopic expression of miR-199a-5p was sufficient to promote the pathogenic activation of pulmonary fibroblasts. CAV1, a critical mediator of pulmonary fibrosis, was established as a bona fide target of miR-199a-5p. Finally, we also found an aberrant expression of miR-199a-5p in mouse models of kidney and liver fibrosis, suggesting that dysregulation of miR-199a-5p represents a general mechanism contributing to the fibrotic process. We propose miR-199a-5p as a major regulator of fibrosis that represents a potential therapeutic target to treat fibroproliferative diseases. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-02-01 | E-GEOD-34818 | biostudies-arrayexpress

SSc biomarkers detection in the secretome of TGF1-activated primary human lung fibroblasts.

Project description:TGFβ1 is a profibrotic mediator that contributes to a broad spectrum of pathologies, including pulmonary fibrosis (PF). However, the secretome of TGFβ1-stimulated primary human normal lung (NL) fibroblasts has not been well characterized. Using fluorescent 2-dimensional gel electrophoresis (2D-PAGE) and differential gel electrophoresis (DIGE), we identified 37 differentially secreted proteins in the conditioned media of TGFβ1-activated NL fibroblasts and generated a protein-protein association network of the TGFβ1 secretome using STRING. Functional enrichment revealed that biological processes and pathways characteristics of PF were enriched. Using the DrugBank database, we determined that 32 of the secreted proteins are targets of known experimental, investigational and approved drugs. Additionally, by comparing the TGFβ1 secretome of NL fibroblasts to proteomic biomarkers from biological fluids of systemic sclerosis (SSc) patients, we identified 11 overlapping proteins. Together our data validate the TGFβ1-induced secretome of NL fibroblasts as a valid in vitro model that reflects SSc biomarkers and identifies potential therapeutic targets for SSc-PF.

2022-08-12 | PXD023862 | Pride

MiR-199a-5p determines fibroblast activation and pulmonary fibrogenesis

2013-02-01 | GSE34818 | GEO

Gene expression profiles of CEBPβ-overexpressed alveolar macrophages after A20-Ad treatment

Project description:Although recent progressions have provided significant mechanistic insights into the pathogenesis of pulmonary fibrosis (PF), few of anti-PF therapeutics show certain promise for this devastating disease. Chronic or repeated lung injury results in chronic inflammation, which functions as a major driven force to promote PF development. Here we report that chronic lung injury inactivates ubiquitin-modifying enzyme A20 to cause a progressive accumulation of transcription factor C/EBPb in macrophages, which produce a number of pro-fibrotic factors to promote PF development. Elevated GSK-3b expression, in response to chronic lung injury, interacts with and phosphorylates A20 to suppress C/EBPb degradation in macrophages. Enforced expression of A20 or pharmacological acceleration of C/EBPb degradation by a peptide restores the A20 activity and provides potent therapeutic efficacy against experimental PF. Our studies reveal a regulatory mechanism of the GSK-3b-A20-C/EBPb axis in alveolar macrophages, by targeting which can treat PF and fibroproliferative lung diseases.

2018-10-01 | GSE117690 | GEO

Gene expression profiles of alveolar macrophages isolated from wild type (WT) and A20 conditional knockout mice after BLM exposure

2018-10-01 | GSE117649 | GEO

Time-series transcriptomic analysis of lung fibroblasts in bleomycin- and silica-induced pulmonary fibrosis

Project description:Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although lung fibroblasts play central roles in PF, their key regulatory molecules remain unclear. To identify PF pathology-associated gene modules and their hub TFs in activated lung fibroblasts, we performed time-course transcriptome analysis of the fibroblasts purified from the lungs of bleomycin- and silica-treated Col1a2-GFP reporter mice.

2019-01-30 | GSE110540 | GEO

Transcriptomic analysis of active form of Srebf1-overexpressed fibroblasts in bleomycin-induced lung fibrosis

Project description:Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although lung fibroblasts play central roles in PF, their key regulatory molecules remain unclear. We performed transcriptome analysis of lung fibroblasts from bleomycin- and silica-treated murine lungs and identified 55 hub transcription factors highly connected to gene modules differentially expressed in PF. To elucidate whether fibroblast-specific intervention against the hub transcription factor Srebf1 modulates pathogenic activation of lung fibroblasts in vivo, we intratracheally-transferred active form of Srebf1-overexpressed fibroblasts into bleomycin-treated lungs and performed global transcriptome analysis.

2019-01-30 | GSE110533 | GEO

Gene induction by Dex, IL-9 and CCL-1 in BW5147 mouse T cell lymphoma

Project description:The aim of this work was to determine the genes and mechanisms involved in IL-9- and CCL1-mediated protection against glucocorticoid-induced apoptosis. We made the hypothesis that the expression of the really critical mediators could be regulated in a reciprocal way by Dex on the one hand and anti-apoptotic cytokines such as IL-9 and CCL1 on the other hand.Therefore, we performed a comprehensive study of the genes expressed by BW5147 cells stimulated with or without Dex, IL-9 and CCL1, taking advantage of the Affymetrix microarray technology. Keywords: cytokine and dexamethasone stimulation One million BW5147 cells were stimulated with 100 ng/ml of dexamethasone and/or with 100 U/ml of IL-9 or CCL1 for eight hours. RNA was then extracted for hybridization on Affymetrix microarrays. This experiment was performed in duplicates .

2011-05-25 | E-GEOD-13823 | biostudies-arrayexpress

microRNA expression profiles of extracellular vehicles released from alveolar macrophage

Project description:Interstitial lung diseases (ILDs) such as idiopathic pulmonary fibrosis (IPF) is diffuse parenchymal lung disorders characterized by varying degrees of inflammation and fibrosis of the lung interstitium. The failure of lung alveolar regeneration in IPF is critical for this incurable disease. Here we report that chronic lung injury causes a profibrotic phenotype of alveolar macrophages that release extracellular vehicles (EVs) to promote PF development through repressing the stemness traits of type 2 alveolar epithelial cells (AEC2s). We found that an increased expression of acetylases KAT5 interacts with and acetylates protein kinase MLKL, which directly promotes release of EVs from AMs following chronic lung injury. AEC2s takes up the EVs and releases miR-148a-3p to repress expression of endogenous b-catennin agonist Wnt10b and alveolar regeneration. Pharmacologic inhibition of the miR-148a-3p expression or interruption of the KAT5-MLKL interaction restores regenerative capacity of AEC2s and exhibits potent therapeutic efficacy against PF. Our study confers a potential strategy for the treatment of IPF and other interstitial lung diseases.

2023-09-01 | GSE184147 | GEO

Gene induction by Dex, IL-9 and CCL-1 in BW5147 mouse T cell lymphoma

2011-05-25 | GSE13823 | 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