MicroRNA expression profiles in Idiopathic Pulmonary Fibrosis (IPF)
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ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE129126 | GEO | 2019/04/02
REPOSITORIES: GEO
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Project description:Visium (10x Genomics) spatially resolved transcriptomics data generated from normal and Idiopathic Pulmonary Fibrosis (IPF) lung parenchyma tissues collected from human donors. The fresh-frozen tissues that were analyzed were from four healthy control (HC) subjects and from four IPF patients. For each IPF patient, three different tissues were selected representing areas of mild (“B1”), moderate (“B2\") or severe (“B3”) fibrosis within the same donor, as determined by histological inspection of Hematoxylin and Eosin (H&E)-stained samples. Data from a total of 25 tissue sections, from 16 unique lung tissue blocks. The lung tissues were collected post-mortem (HC donors) or during lung transplant/resection (IPF patients) after obtaining informed consent. The study protocols were approved by the local human research ethics committee (HC: Lund, permit number Dnr 2016/317; IPF: Gothenburg, permit number 1026-15) and the samples are anonymized and cannot/should not be traced back to individual donors.
2024-05-28 | E-MTAB-14121 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is a disease related to AT2 cell. We used flow cytometry to analyze the epithelial component of donor and IPF lungs. From the live cells, we first excluded the CD31PosCD45Pos and then selected the EPCAMPos cells for further analysis using the human AT2 cell marker HTll-280 and the surface marker PD-L1. Our data indicate that, the bona fide differentiated AT2 cells (HTll-280High PD-L1Neg), were drastically reduced in the context of IPF. More interestingly, the number of HTll-280Low/Neg PD-L1High was drastically increased, suggesting that HTll-280Low PD-L1High epithelial cells could represent a pool of progenitors linked to the deficient AT2 lineage. The aim of this experiment is further characterization of AT2 and PDL1+ cells in donor and IPF.
2023-01-01 | GSE195770 | 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:Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition. The expression and role of microRNAs (miRNA) has not been studied in IPF. Using miRNA expression microarrays we identified 46 differentially expressed miRNA in IPF lungs which included let-7d and the miR-30 family. Keywords: miRNA expression Lung tissue samples for microarray analysis were obtained through the University of Pittsburgh Health Sciences Tissue Bank. Ten samples were obtained from surgical remnants of biopsies or lungs explanted from patients with IPF who underwent pulmonary transplant, and ten control normal lung tissues obtained from the disease free margins with normal histology of lung cancer resection specimens. The morphologic diagnosis of IPF was based on typical microscopic findings consistent with usual interstitial pneumonia. Total RNA was labeled with Cy3 and hybridized on Agilent 8X15K microRNA array (Agilent Technologies, Santa Clara, CA). After 20 hours hybridization, arrays were washed and scanned according to the manufacturerâs protocol.
2010-04-23 | E-GEOD-13316 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is an untreatable fibrotic lung disease characterized by fibroblast proliferation and epithelial mesenchymal transition. Using miRNA expression microarrays we identified 96 differentially expressed miRNA in IPF lungs which included let-7d, miR-30 family, miR-29 family and miR-154 family. Lung tissue samples for microarray analysis were obtained through the University of Pittsburgh Health Sciences Tissue Bank. 13 samples were obtained from surgical remnants of biopsies or lungs explanted from patients with IPF who underwent pulmonary transplant, and 12 control normal lung tissues obtained from the disease free margins with normal histology of lung cancer resection specimens. The morphologic diagnosis of IPF was based on typical microscopic findings consistent with usual interstitial pneumonia. Total RNA was labeled with Cy3 and hybridized on Agilent 8X15K microRNA array (Agilent Technologies, Santa Clara, CA). After 20 hours hybridization, arrays were washed and scanned according to the manufacturer’s protocol.
2013-01-04 | E-GEOD-27430 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic fibrosing lung disease that is difficult to diagnose and follows an unpredictable clinical course. The object of this study was to develop a predictive gene signature model of IPF from whole lung tissue. We collected whole lung samples from 11 IPF patients undergoing diagnostic surgical biopsy or transplantation. Whenever possible, samples were obtained from different lobes. Normals consisted of healthy organs donated for transplantation. We measured gene expression on microarrays. Data were analyzed by hierarchical clustering and Principal Component Analysis. By this approach, we found that gene expression was similar in the upper and lower lobes of individuals with IPF. We also found that biopsied and explanted specimens contained different patterns of gene expression; therefore, we analyzed biopsies and explants separately. Signatures were derived by fitting top genes to a Bayesian probit regression model. We developed a 153-gene signature that discriminates IPF biopsies from normal. We also developed a 70-gene signature that discriminates IPF explants from normal. Both signatures were validated on an independent cohort. The IPF Biopsy signature correctly diagnosed 76% of the validation cases (p < 0.01), while IPF Explant correctly diagnosed 78% (p < 0.001). Examination of differentially expressed genes revealed partial overlap between IPF Biopsy and IPF Explant and almost no overlap with previously reported IPF gene lists. However, several overlapping genes may provide a basis for developing therapeutic targets. 17 samples from 11 patients with IPF (6 patients provided a pair of samples from upper and lower lobes; 5 patients contributed singleton samples); 6 control specimens were obtained from routine lung volume reduction of healthy donor lungs at the time of lung transplantation.
2011-11-01 | E-GEOD-24206 | biostudies-arrayexpress
Project description:Accelerated senescence in lung epithelial cells is known to play a key role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, the exact mechanisms underlying the IPF-related epithelial cell phenotype have yet to be elucidated. Increasing evidence supports the concept that extracellular vesicles (EVs), including exosomes and microvesicles, mediate intercellular communication that contributes to diverse aspects of physiology and pathogenesis. Here, we demonstrate that lung fibroblasts (LFs) from IPF patients accelerate epithelial cell senescence via EV-mediated transfer of LF-derived pathogenic cargo to lung epithelial cells. Mechanistically, IPF LF-derived EVs increase mitochondrial reactive oxygen species (mtROS) and associated mitochondrial damage in lung epithelial cells, leading to mtROS-mediated activation of the DNA damage response and subsequent epithelial cell senescence. We show that IPF LF-derived EVs contain elevated levels of miR-23b-3p and miR-494-3p that are responsible for suppressing SIRT3, resulting in the EV-induced phenotypic changes of lung epithelial cells. Furthermore, we observe that miR-23b-3p and miR-494-3p expression increases in lung epithelial cells from IPF patients’ lungs. Finally, the levels of miR-23b-3p and 494-3p found in IPF LF-derived EVs correlate positively with IPF disease severity. These findings reveal that the accelerated epithelial cell mitochondrial damage and senescence observed during IPF pathogenesis are caused by a novel mechanism in which SIRT3 is suppressed by miR-containing EVs derived from IPF fibroblasts.
2020-08-04 | GSE124665 | GEO
Project description:Analysis of gene expression of lung fibroblasts seeded onto decellularized extracellular matrix (ECM). Experiment had 2x2 design where fibroblasts from idiopathic pulmonary fibrosis (IPF) or control patients were seeded onto decelluarized lung tissue from IPF or control patients allowing for determination of gene expression differences that were driven by IPF ECM and which differences were driven by the IPF fibroblast. Lung fibroblasts from 5 patients with idiopathic pulmonary fibrosis and 5 control patients were cultured on decellularized ECM from IPF or control lung. Total RNA and polyribosome RNA were isolated after the cells were cultured on the decellularized ECM for 18 hours. When possible, a control cell line and a diseased cell line were cultured (and processed) simultaneously to minimize the effect of experimental variance induced by running the experiment at different times.Samples with the same batch number (provied in the sample 'characteristics' field) were cultured and processed at the same time.
2014-03-04 | E-GEOD-45686 | biostudies-arrayexpress
Project description:Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive fibrosing interstitial lung disease that is unresponsive to current therapy. While it carries a median survival of less than 3 years its rate of progression varies widely between patients. We hypothesized that studying the gene expression profiles of physiologically stable patients and those in which the disease progressed rapidly after the initial diagnosis would aid in the search for biomarkers and contribute to the understanding of disease pathogenesis. We generated 12 Idiopathic Pulmonary Fibrosis (IPF) lung parenchyma SAGE profiles. Initial cluster analysis including 8 other public available lung SAGE libraries verified that the IPF transcriptome is distinct from normal lung tissue and other lung diseases like COPD. In order to identify candidate markers of disease progression we segregated the IPF SAGE profiles in two groups based on clinical parameters regarding lung volume and lung function.
2009-04-07 | E-GEOD-11665 | biostudies-arrayexpress
Project description:There is microscopic spatial and temporal heterogeneity of pathologic changes in idiopathic pulmonary fibrosis (IPF) lung tissue, which may relate to heterogeneity in pathophysiological mediators of disease and clinical progression. We measured gene expression in samples from lung biopsies or explants in order to assess relationships with pathological features and systemic biomarkers. RNA was extracted directly from lung tissue samples from 40 IPF patients or 8 healthy controls.
2014-10-14 | E-GEOD-53845 | biostudies-arrayexpress