Gene expression in lung fibroblasts
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE10921 | GEO | 2009/03/19
SECONDARY ACCESSION(S): PRJNA107225
REPOSITORIES: GEO
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Project description:Pulmonary fibrosis is a chronic, progressive, and lethal interstitial lung disease. It is characterized by extracellular matrix deposition, fibroblast proliferation, and accumulation. Fibroblasts from normal or UIP histology were cultured and analyzed. Keywords: Fibroblasts from normal histology lung tissue or UIP histology lung tissue Five samples of primary human lung fibroblasts were obtained from explanted lungs of patients with Usual Interstitial Pneumonia (UIP) at the University of Pittsburgh Medical Center (Pittsburgh, PA, USA) and three samples of primary normal human lung fibroblasts were acquired from normal histololgy lung tissues of organ donors. The experimental protocol was approved by the University of Pittsburgh Institutional Reviews Board (IRB). Total RNA was extracted and used as a template to generate double-stranded cDNA and biotin-labeled cRNA, as recommended by the manufacturer of the arrays. Fragmented cRNA was hybridized to Codelink Uniset I slides. After hybridization, arrays were washed and stained with streptavidin-AlexaFluor 647. The arrays were scanned using a Genepix 4000B microarray scanner. Images were analyzed using Codelink expression II analysis suite, and visually inspected for defects and quality control parameters as recommended by the manufacturer.
2010-06-21 | E-GEOD-10921 | biostudies-arrayexpress
Project description:Rationale: Idiopathic interstitial pneumonia (IIP) and its’ familial variants are progressive and largely untreatable disorders with poorly understood molecular mechanisms. Both the genetics and the histologic type of IIP play a role in understanding the etiology and pathogenesis of interstitial lung disease, but transcriptional signatures of these subtypes are unknown. Objectives: To evaluate gene expression in the lung tissue from patients with usual interstitial pneumonia (UIP) and non-specific interstitial pneumonia (NSIP) that were either familial or non-familial in origin and compare them to gene expression from normal lung parenchyma. Methods: We profiled RNA from lungs of 16 patients with sporadic IIP, 10 with familial IIP, and 9 normal controls on a whole human genome oligonucleotide microarray. Results: Significant transcriptional differences exist in familial and sporadic IIPs. The genes distinguishing the genetic subtypes belong to the same functional categories as transcripts that distinguish IIP from normal samples. Relevant categories include chemokines and growth factors and their receptors, complement components, genes associated with cell proliferation and death, and genes in the Wnt pathway. Keywords: disease state analysis
2006-10-01 | GSE5774 | GEO
Project description:Purpose: The goal of this study is to compare transcriptome profiling (RNA-seq) of lung tissue biopsies derived from patients with idiopathic pulmonary fibrosis (IPF or IPF-UIP), or rheumatoid arthritis-associated interstitial diseases (RA-ILD or RA-UIP), or non-usual interstitial pneumonia (non-UIP) controls. Methods: Total RNA was extracted using the RNeasy kit (Qiagen) from fresh frozen lung tissue obtained from the Lung Tissue Repository Consortium (LTRC). RNA samples were then sent to the Genome Analysis Core at Mayo Clinic for sequencing using conventional Illumina mRNA-Seq protocols. A total of 23,295 genes were probed using this platform. Results: RNA-seq data revealed considerable transcriptomic differences between the groups. A heat map generated with the most differentially expressed genes (P<0.05) revealed two distinct gene expression profiles among the three groups. The heat map for the 3 RA-UIP and 20 IPF patients showed a similar gene expression pattern, which contrasted significantly from the non-UIP control group. Conclusions: The RNA-Seq data analysis shows similarities and differences between gene expression profiles of RA-UIP and IPF, suggesting both shared and differential disease-causing mechanistic pathways. Transcriptomic data distinguishes the RA-UIP group from IPF via JAK2-related JAK/STAT signaling pathways.
2022-05-31 | GSE199152 | GEO
Project description:Pulmonary fibrosis develops as a consequence of environmentally induced lung injury and/or an inherent disease susceptibility causing fibroblast activation, proliferation and extracellular matrix deposition. The study was undertaken to characterise global gene expression in pulmonary fibroblasts to better understand the mechanisms underlying the fibrotic fibroblast phenotype. Gene expression was evaluated in lung fibroblasts derived from ten controls (normal periphery of resected tumor), open lung biopsies from eight patients with interstitial lung disease associated with systemic sclerosis (fibrotic non specific interstitial pneumonia pattern on biopsy), and from three patients with usual interstitial pneumonia. Lung fibroblasts were grown to confluence in DMEM with 10% fetal calf serum. At confluence, lung fibroblasts were serum-deprived for 44 hours in the presence of fibroblast growth medium with the addition of 0.1% bovine serum albumin (Sigma).
2013-08-05 | E-GEOD-40839 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive lethal interstitial lung disease of unkown etiology with limited effective therapies. The pathogenic mechanisms of IPF remain unkown. Emerging evidences indicate that abnormal behaviors of fibroblasts in IPF are associated with a variety of genetic alterations and aberrant reactivation of developmental signaling pathways. We compared gene expression profiles in fibrotic lung tissues from IPF patients and normal lung tissues from patients with primary spontaneous pneumothorax using cDNA microarray to examine the mechnisms involved in the pathogenesis of IPF.
2015-08-15 | GSE72073 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic progressive fibrosing interstitial pneumonia leading to progressive dyspnea and finally death.The classic diagnosis of IPF is based on the histological pattern of usual interstitial pneumonia (UIP).we have no information about the molecular events that characterize the progression of IPF in the human lung. Understanding the molecular changes that characterize the progression of IPF from early, through progressive changes and into end-stage would allow development of therapeutic strategies that address the disease in all of its stages.In this study we applied a systems biology approach to model dynamic molecular changes during the progression of IPF in the human lung by using a unique resource of carefully characterized, differentially affected regions in human lungs.
2019-10-11 | GSE124685 | GEO
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and usually lethal lung disease characterized by unknown causes and few treatment options We used microarray to determine the expression of miRNA and 17 miRNAs were differentially expressed in IPF lungs, including 10 upregulated and 7 downregulated miRNAs. Lung tissue was obtained from 4 IPF patients with histological evidence of usual interstitial pneumonia at the time of surgical lung biopsy or lung transplantation. The diagnosis of IPF was derived according to the standards accepted by the American Thoracic Society/European Respiratory Society. Histological normal lung tissues used as controls was obtained from 3 patients with primary spontaneous pneumothorax at the time of thoracoscopy with stapling of any air leak.The miRNA expression profile was determined by Affymetrix microarray, and transcriptome with Affymetrix array
2015-12-04 | E-GEOD-75647 | biostudies-arrayexpress
Project description:The mechanisms and molecular pathways underlying interstitial lung diseases (ILDs) are poorly understood. Systems biology approaches were used to identify perturbed networks in these disease states to gain a better understanding of the underlying mechanisms of disease. Through profiling genes and miRNAs, we found subsets of genes and miRNAs that distinguish different disease stages, ILDs from controls, and idiopathic pulmonary fibrosis (IPF) from non-specific interstitial pneumonitis (NSIP). Traditional pathway analysis revealed several disease-associated modules involving genes from the TGF-beta, Wnt, focal adhesion and smooth muscle actin pathways that may be involved in advancing fibrosis. A comprehensively integrative approach was used to construct a global gene regulatory network based on the perturbation of key regulatory elements, transcriptional factors and miRNAs. The data also demonstrated that several subnetworks were significantly associated with key molecules involved in the diseases. We present a broad overview of the disease at a molecular level and discuss several possibly key regulatory molecular circuits that could play central roles in facilitating the progression of ILDs. Lung tissue samples from 23 patients with IPF or related disorders were obtained from the Lung Tissue Research Consortium (www.ltrcpublic.org). 11 samples came from patients who had been diagnosed with usual interstitial pneumonia/ idiopathic pulmonary fibrosis (UIP/IPF), 5 samples came from patients with non-specific interstitial pneumonia (NSIP), the remaining from patients with uncharacterized fibrosis and from patients with other ILD variants. B. Biopsies from uninvolved lung tissue from lung cancer patients (5 samples) and from one lung transplant patient were used as controls for comparison with the ILD samples.
2011-03-24 | E-GEOD-21369 | biostudies-arrayexpress
Project description:The mechanisms and molecular pathways underlying interstitial lung diseases (ILDs) are poorly understood. Systems biology approaches were used to identify perturbed networks in these disease states to gain a better understanding of the underlying mechanisms of disease. Through profiling genes and miRNAs, we found subsets of genes and miRNAs that distinguish different disease stages, ILDs from controls, and idiopathic pulmonary fibrosis (IPF) from non-specific interstitial pneumonitis (NSIP). Traditional pathway analysis revealed several disease-associated modules involving genes from the TGF-beta, Wnt, focal adhesion and smooth muscle actin pathways that may be involved in advancing fibrosis. A comprehensively integrative approach was used to construct a global gene regulatory network based on the perturbation of key regulatory elements, transcriptional factors and miRNAs. The data also demonstrated that several subnetworks were significantly associated with key molecules involved in the diseases. We present a broad overview of the disease at a molecular level and discuss several possibly key regulatory molecular circuits that could play central roles in facilitating the progression of ILDs. Lung tissue samples from thirty patients with IPF or related disorders were obtained from the Lung Tissue Research Consortium (www.ltrcpublic.org). Ten samples came from patients who had been diagnosed with usual interstitial pneumonia/ idiopathic pulmonary fibrosis (UIP/IPF), nine samples came from patients with non-specific interstitial pneumonia (NSIP), four from patients with uncharacterized fibrosis, and the remaining samples came from patients with other ILD variants. Biopsies from uninvolved lung tissue from lung cancer patients (5 samples) and from one lung transplant patient were used as controls for comparison with the ILD samples.
2011-04-19 | E-GEOD-21394 | biostudies-arrayexpress
Project description:Progressive tissue fibrosis is a major cause of morbidity, and idiopathic pulmonary fibrosis (IPF) is a terminal illness characterized by unremitting matrix deposition in the lung with very limited choice of therapies. The imcomplete understanding of the mechanisms of progressive fibrosis curbs the progress in therapeutics development. Of which, the origin of fibrotic fibroblasts has been poorly defined during the pathogenesis of tissue fibrosis. Here, we fate-mapped a early embryonic transcription factor T-box gene 4 (Tbx4)-derived mesenchymal progenitors in injured adult lung and found that Tbx4+ lineage cells are the major source of myofibroblasts. The ablation of Tbx4+ cells or disruption of Tbx4 signaling attenuated lung fibrosis in bleomycin injury model in mice in vivo. Furthermore, Tbx4+ fibroblasts are more invasive and the regulation of fibroblast invasiveness by Tbx4 is through mediating hyaluronan synthase 2 (HAS2). This study identified a major mesenchymal transcription factor driving the development of fibrotic fibroblasts during lung fibrosis. Understanding the origin, signaling, and functions of these fibroblasts would prove pivotal in the development of therapeutics for patients with progressive fibrotic diseases. We used microarrays to detail the gene expression of Tbx4 and non-Tbx4 cultured fibroblasts.
2017-08-23 | GSE68427 | GEO