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Transforming growth factor beta 1 induces methylation changes in lung fibroblasts [Illumina]

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a complex disease of unknown etiology. Environmental factors can affect disease susceptibility via epigenetic effects. Few studies explore global DNA methylation in lung fibroblasts, but none have focused on transforming growth factor beta-1 (TGF-b1) as a potential modifier of the DNA methylome. Here we analyzed changes in methylation and gene transcription in normal and IPF fibroblasts following TGF-b1 treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE135097 | GEO | 2019/07/31

REPOSITORIES: GEO

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Transforming growth factor beta 1 induces methylation changes in lung fibroblasts [Affymetrix]

Project description:Idiopathic pulmonary fibrosis (IPF) is a complex disease of unknown etiology. Environmental factors can affect disease susceptibility via epigenetic effects. Few studies explore global DNA methylation in lung fibroblasts, but none have focused on transforming growth factor beta-1 (TGF-b1) as a potential modifier of the DNA methylome. Here we analyzed changes in methylation and gene transcription in normal and IPF fibroblasts following TGF-b1 treatment.

2019-07-31 | GSE135065 | GEO

Transforming growth factor beta 1 induces methylation changes in lung fibroblasts

Project description:This SuperSeries is composed of the SubSeries listed below. Idiopathic pulmonary fibrosis (IPF) is a complex disease of unknown etiology. Environmental factors can affect disease susceptibility via epigenetic effects. Few studies explore global DNA methylation in lung fibroblasts, but none have focused on transforming growth factor beta-1 (TGF-b1) as a potential modifier of the DNA methylome. Here we analyzed changes in methylation and gene transcription in normal and IPF fibroblasts following TGF-b1 treatment.

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Role of mTOR in regulating the extra cellular matrix

Project description:Explored the potential role of mTOR in regulating the extra cellular matrix of TGF-b1-stimulated IPF fibroblasts grown under macromolecular crowding conditions in the presence of either CZ415 or rapamycin

2018-11-04 | PXD010164 | Pride

Long intergenic non-coding RNAs regulate human lung fibroblast function: Implications for idiopathic pulmonary fibrosis [ChIP-seq]

Project description:Phenotypic changes in lung fibroblasts are believed to contribute to the development of Idiopathic Pulmonary Fibrosis (IPF), a progressive and fatal lung disease. Long intergenic non-coding RNAs (lincRNAs) have been identified as novel regulators of gene expression and protein activity. In non-stimulated cells, we observed reduced proliferation and inflammation but no difference in the fibrotic response of IPF fibroblasts. These functional changes in non-stimulated cells were associated with changes in the expression of the histone marks, H3K4me1, H3K4me3 and H3K27ac indicating a possible involvement of epigenetics. Following activation with TGF-b1 and IL-1b, we demonstrated an increased fibrotic but reduced inflammatory response in IPF fibroblasts. There was no significant difference in proliferation following PDGF exposure. The lincRNAs, LINC00960 and LINC01140 were upregulated in IPF fibroblasts. Knockdown studies showed that LINC00960 and LINC01140 were positive regulators of proliferation in both control and IPF fibroblasts but had no effect upon the fibrotic response. Knockdown of LINC01140 but not LINC00960 increased the inflammatory response, which was greater in IPF compared to control fibroblasts. Overall, these studies demonstrate for the first time that lincRNAs are important regulators of proliferation and inflammation in human lung fibroblasts and that these might mediate the reduced inflammatory response observed in IPF-derived fibroblasts.

2019-03-31 | GSE129085 | GEO

Transcriptome analysis of lung fibroblasts from 5 control and 5 IPF patients with/out TGF-b1 stimulation

Project description:Isolated primary human fibroblasts from 5 control and 5 IPF patients were treated with/out 3ng/ml TGF-b1 for 24 hours before cells were lysed for RNA extraction.

2019-04-02 | GSE129164 | GEO

Identification of the gene expression in IPF lung fibroblasts after demethylation

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease. Although the pathogenesis is poorly understood, evidence suggests that genetic and epigenetic alterations, such as DNA methylation, may play a key role. We used microarrays to see the gene expression in IPF fibroblasts after demethylation agent 5'-azacytidine treatment. Human IPF lung fibroblasts were cultured and then treated with 5'-azacytidine 5uM 24 hours. RNA were extracted and hybridized on Affymetrix microarrays.

2016-02-16 | E-GEOD-69764 | biostudies-arrayexpress

To examine the expression of Sulf1 and Sulf2, as well as other glycan-related genes, in human Idiopathic pulmonary fibrosis (IPF) lungs compared to normal lung samples

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Bi-directional epithelial-mesenchymal crosstalk provides self-sustaining pro-fibrotic signals in pulmonary fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is the prototypic progressive fibrotic lung disease with a median survival of 2-4 years. Injury to and/or dysfunction of alveolar epithelium are strongly implicated in IPF disease initiation, but what factors determine why fibrosis progresses rather than normal tissue repair occurs remain poorly understood. We previously demonstrated that ZEB1-mediated epithelial-mesenchymal transition (EMT) in human alveolar epithelial type II (ATII) cells augments TGF-β-induced profibrogenic responses in underlying lung fibroblasts by paracrine signalling. Here we investigated bi-directional epithelial-mesenchymal crosstalk and its potential to drive fibrosis progression. RNA sequencing (RNA-seq) of lung fibroblasts exposed to conditioned media from ATII cells undergoing RAS-induced EMT identified many differentially expressed genes including those involved in cell migration and extracellular matrix (ECM) regulation. We confirmed that paracrine signalling between AS-activated ATII cells and fibroblasts augmented fibroblast recruitment and demonstrated that this involved a ZEB1-tissue plasminogen activator (tPA) axis. In a reciprocal fashion, paracrine signalling from TGF-β-activated lung fibroblasts or IPF fibroblasts induced RAS activation in ATII cells, at least partially via the secreted protein, SPARC. Together these data identify that aberrant bi-directional epithelial-mesenchymal crosstalk in IPF drives a chronic feedback loop that maintains a wound-healing phenotype and provides self-sustaining pro-fibrotic signals.

2021-08-19 | PXD025821 | Pride

Identification of the gene expression in IPF lung fibroblasts after demethylation

2016-02-16 | GSE69764 | GEO

Global Gene Expression Profiles of Fibroblasts from the Lungs of Patients with Idiopathic Pulmonary Fibrosis: The Role of CCL8

Project description:Analysis of Idiopathic pulmonary fibrosis (IPF) at gene expression level. The hypothesis tested in the present study was that Epigenetic mechanisms are likely to be associated with pathogenesis in IPF. To determine the DNA methylation change, and their effects on gene expression, we compared microarray data of DNA methylation and RNA expression. Results provide that among the genes whose DNA methylation status and RNA expression were both significantly altered between IPF-rapid and normal controls. Total RNA obtained from Idiopathic pulmonary fibrosis samples.

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