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.

2017-11-22 | GSE107226 | GEO

Global methylation patterns in idiopathic pulmonary fibrosis.

Project description: Not available

| S-EPMC3323629 | biostudies-literature

Global Methylation Patterns in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a chronic progressive lung disease that affects more than 5 million people worldwide with a steady increase in both incidence and mortality. There is currently no effective therapy and the median survival without transplant is 2-5 years. The etiological factor is unknown, but several observational and pathogenesis studies suggest that environmental agents may cause IPF. DNA methylation is a type of chemical modification of DNA such environmental and occupational factors, that can induced a changes in the regulation of biological processes and link to diseases such as a cancer. We hypothesize that the global changes in methylation patterns of IPF lungs caused by environmental factors. In this study we will identify the global methylation signatures of the IPF lung and to compare to methylation signature of lung cancer. The DNA methylation profiles of IPF lung tissue differs from control lung but it shares great similarity with that of lung cancer. Immunoprecipitated methylated DNA from 12 IPF lungs, 10 lung adenocarcinomas and 10 normal histology lungs obtained from the same group of adenocarcinoma patients was hybridized to Agilent human CpG Islands Microarrays. Only probes with a hybridization Tm value between 79 C and 93C were included in the analysis because these show higher quality signal. All probes were divided according to their Tm into 14 groups/bins differing by 1C. Probe signals in each bin were standardized to have an average of 0 and a standard deviation of 1. To work in a CpG island oriented manner, we scored each island for its likelihood to be methylated. For that purpose, each probe was mapped to the genome and the signals of the probes that were mapped to a single CpG island were averaged to obtain the islandM-bM-^@M-^Ys methylation score. Data analysis was performed using BRB-Array Tools and DAVID Bioinformatics Resources software packages.

2012-04-18 | E-GEOD-29895 | biostudies-arrayexpress

Altered epigenetic features in circulating nucleosomes in idiopathic pulmonary fibrosis.

Project description: Not available

| S-EPMC5558769 | biostudies-other

Molecular Signatures of Idiopathic Pulmonary Fibrosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-09 | GSE173357 | GEO

Global DNA Methylation Levels in Lung Fibroblasts from Patients with Idiopathic Pulmonary Fibrosis Compared to Nonfibrotic Controls

Project description:Fibroblasts are the key effector cells in idiopathic pulmonary fibrosis (IPF), a chronic, progressive scarring disorder that results in impaired gas exchange and respiratory failure. Fibroblasts from IPF patients exhibit aberrant expression of multiple genes, but the DNA methylome of IPF fibroblasts has never been characterized. We utilized the HumanMethylation27 array, which assays the DNA methylation level of 27,568 CpG sites to compare the DNA methylation patterns of IPF fibroblasts (n=6) with those of nonfibrotic patient controls (n=3) and commercially available normal lung fibroblast cell lines (CCL190, CCL204, and CCL210). Multiple CpG sites across the genome were differentially methylated (as defined by P value less than 0.05 and fold change greater than 2) in IPF fibroblasts compared to fibroblasts from nonfibrotic controls. These methylation changes occurred in both genes recognized to be important in fibroproliferation and extracellular matrix generation, as well as in genes not previously recognized to participate in those processes (including organ morphogenesis and potassium ion channels). We used bisulfite sequencing to independently verify DNA methylation changes in 3 genes (CDKN2B, CARD10, and MGMT); these methylation changes corresponded with changes in gene expression at the mRNA and protein level. These changes in DNA methylation were stable throughout multiple cell passages. DNA methylation changes may thus help to explain a proportion of the differences in gene expression previously observed in studies of IPF fibroblasts. Moreover, significant variability in DNA methylation was observed among individual IPF cell lines, suggesting that differences in DNA methylation may contribute to fibroblast heterogeneity among patients with IPF. These results demonstrate that IPF fibroblasts exhibit global differences in DNA methylation that may contribute to the excessive fibroproliferation associated with this disease.

2014-12-01 | GSE56074 | GEO

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