Results of differentially expressed lncRNAs in COPD and healthy smoker using the Arraystar Human LncRNA Microarray
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE107426 | GEO | 2017/11/29
SECONDARY ACCESSION(S): PRJNA420055
REPOSITORIES: GEO
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Project description:With the aim of exploring expression profiles and biological functions of long non-coding RNA (lncRNA) and mRNAs after ischemia-reperfusion injury (SCII), differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) in rat spinal cords were identified following SCII through high-throughput RNA sequencing. In total, 1455 lncRNAs and 6707 mRNAs were observed to be differentially expressed (FC ≥1.5 and P <0.05) after SCII, including 761 up-regulated and 694 down-regulated lncRNAs and, 3772 up-regulated and 2935 down-regulated mRNAs.
2019-12-08 | GSE138966 | GEO
Project description:Results of differentially expressed lncRNAs in COPD and healthy smoker using the Arraystar Human LncRNA Microarray
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Project description:Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, we identified a novel subpopulation of Alveolar Type 2 epithelial cells that emerged in smokers, such as COPD patients, and specifically expressed a series of chemokines and PD-L1. Since the number of cells in the basal cell clusters increased in only the COPD lungs but not in the non-COPD smoker or never-smoker lungs, we also tried to clarify the difference in phenotype between COPD and other basal cells with single-cell RNA-seq. However, due to the small number of cells in each, no clear difference could be found. To further investigate the functional properties of basal cells in COPD, we isolated small airway epithelial cells from surgical samples of COPD or never-smoker lungs and expanded the cells in vitro.Total RNA was extracted from early passaged cells , and bulk RNA-seq was performed to characterize these cells in detail. Finally, we found that the COPD basal cells retained the inflammatory response and basal/stem-related signals, even after a few passages in culture, and it might cause basal cell expansion in vivo.
2021-06-10 | GSE162154 | GEO
Project description:The role of eosinophilic inflammation in chronic obstructive pulmonary disease (COPD) pathogenesis is unknown and is probably different than in asthma. The molecular processes underlying the differences between eosinophils from asthma and COPD have not been studied. The study group included 5 patients with asthma and 4 patients with COPD. The RNA-Seq data analysis identified 26 differentially expressed genes between COPD and asthma (according to adjusted p-value). In total, 6 genes were up-regulated (CCL3L1, CCL4L2, SERPINB2, PRSS21, GPR82) and 20 were down-regulated (e.g. JUN, IFITM3, DUSP1, GNG7, ZNF107, BCL6) in peripheral eosinophils of COPD patients compared to asthma. Biological processes associated with down-regulated genes were cell differentiation, positive regulation of RNA metabolic process. The genes associated with signaling of IL-4 and IL-13 pathway were down-regulated in COPD eosinophils compared to asthma. Peripheral eosinophils from COPD and asthma patients present different transcriptomic profiles suggesting their different function in pathobiology of both obstructive airway diseases.
2024-01-01 | GSE237284 | GEO
Project description:70 miRNAs and 2667 mRNAs were differentially expressed between lung tissue from subjects with COPD and smokers without COPD. miRNA and mRNA expression profiles enriched for biological pathways that may be relevant to the pathogenesis of COPD including the transforming growth factor b, Wnt and focal adhesion pathways. miR-223 and miR-1274a were the most affected miRNAs in subjects with COPD compared with smokers without obstruction. miR-15b was increased in COPD samples compared with smokers without obstruction and localised to both areas of emphysema and fibrosis. miR-15b was differentially expressed within GOLD classes of COPD. Expression of SMAD7, which was validated as a target for miR-15b, was decreased in bronchial epithelial cells in COPD.
2012-06-27 | GSE38974 | GEO
Project description:Study Smoking and COPD are associated with decreased mucociliary clearance and healthy smokers have shorter cilia in the large airway than nonsmokers. Intraflagellar transport (IFT) is the process by which cilia are produced and maintained. We assessed expression of IFT-related genes in smokers and nonsmokers and evaluated cilia length in the large and small airway of nonsmokers, healthy smokers, and smokers with COPD. Methods Airway epithelium was obtained via bronchoscopic brushing. Affymetrix microarrays were used to evaluate IFT gene expression in 2 independent data sets from large and small airway. Cilia length was assessed by measuring 100 cilia (10 cilia on each of 10 cells) per subject. Results All 40 IFT genes were expressed in the human large and small airway epithelium. In the large airway, 10 IFT genes were down-regulated and 1 up-regulated in smokers. In the small airway, 11 genes were down-regulated and 3 up-regulated in smokers. A set of 8 IFT genes was down-regulated in both data sets. In the large and small airway epithelium, cilia were significantly shorter in healthy smokers than nonsmokers, and significantly shorter in COPD smokers than in both healthy smokers and nonsmokers. Answer to the Question These results support the concept that loss of cilia length contributes to defective mucociliary clearance in COPD, and that smoking-induced changes in expression of IFT genes may be one mechanism of abnormally short cilia in smokers. Strategies to normalize cilia length may be an important avenue for novel COPD therapies.
2014-02-03 | GSE43939 | GEO
Project description:70 miRNAs and 2667 mRNAs were differentially expressed between lung tissue from subjects with COPD and smokers without COPD. miRNA and mRNA expression profiles enriched for biological pathways that may be relevant to the pathogenesis of COPD including the transforming growth factor b, Wnt and focal adhesion pathways. miR-223 and miR-1274a were the most affected miRNAs in subjects with COPD compared with smokers without obstruction. miR-15b was increased in COPD samples compared with smokers without obstruction and localised to both areas of emphysema and fibrosis. miR-15b was differentially expressed within GOLD classes of COPD. Expression of SMAD7, which was validated as a target for miR-15b, was decreased in bronchial epithelial cells in COPD. Lung tissue from smokers with no evidence of obstructive lung disease and smokers with COPD was examined for miRNA and mRNA expression followed by validation. We then examined both miRNA and mRNA expression to enrich for relevant biological pathways
2012-06-26 | E-GEOD-38974 | biostudies-arrayexpress
Project description:Background: Chronic obstructive pulmonary disease (COPD) is a major risk factor for the development of lung adenocarcinoma (AC). AC often develops on underlying COPD, thus the differentiation of both entities by biomarker is challenging. Although survival of AC patients strongly depends on early diagnosis, a biomarker panel for AC detection and differentiation from COPD is still missing. Methods: Plasma samples from 176 patients with AC with or without underlying COPD, COPD patients, and hospital controls were analyzed using mass spectrometry-based proteomics. We performed univariate statistics and additionally evaluated machine learning algorithms regarding the differentiation of AC vs. COPD and AC with COPD vs. COPD. Results: Univariate statistics revealed significantly regulated proteins that were significantly regulated between the patient groups. Furthermore, Random forest classification yielded the best performance for differentiation of AC vs. COPD (area under the curve (AUC) 0.935) and AC with COPD vs. COPD (AUC 0.916). The most influential proteins were identified by permutation feature importance and compared to those identified by univariate testing. Conclusion: We demonstrate the great potential of machine learning for differentiation of highly similar disease entities and present a panel of biomarker candidates that should be considered for the development of a future biomarker panel.
2022-10-17 | PXD035120 | Pride
Project description:Genome-wide analysis of lncRNA expression profiles in COPD rat model exposed by cigarette smoking (CS) and fine particulate matter (PM2.5). Goal was to explore the differences and similarities lncRNAs expression in rats model of COPD exposed by CS and PM2.5.
2021-06-21 | GSE178513 | GEO
Project description:Study Smoking and COPD are associated with decreased mucociliary clearance and healthy smokers have shorter cilia in the large airway than nonsmokers. Intraflagellar transport (IFT) is the process by which cilia are produced and maintained. We assessed expression of IFT-related genes in smokers and nonsmokers and evaluated cilia length in the large and small airway of nonsmokers, healthy smokers, and smokers with COPD. Methods Airway epithelium was obtained via bronchoscopic brushing. Affymetrix microarrays were used to evaluate IFT gene expression in 2 independent data sets from large and small airway. Cilia length was assessed by measuring 100 cilia (10 cilia on each of 10 cells) per subject. Results All 40 IFT genes were expressed in the human large and small airway epithelium. In the large airway, 10 IFT genes were down-regulated and 1 up-regulated in smokers. In the small airway, 11 genes were down-regulated and 3 up-regulated in smokers. A set of 8 IFT genes was down-regulated in both data sets. In the large and small airway epithelium, cilia were significantly shorter in healthy smokers than nonsmokers, and significantly shorter in COPD smokers than in both healthy smokers and nonsmokers. Answer to the Question These results support the concept that loss of cilia length contributes to defective mucociliary clearance in COPD, and that smoking-induced changes in expression of IFT genes may be one mechanism of abnormally short cilia in smokers. Strategies to normalize cilia length may be an important avenue for novel COPD therapies. Gene expression was assessed for 40 intraflagellar transport related genes in the LAE of nonsmokers (n=21) and healthy smokers (n=31) and the SAE of an independent group of nonsmokers (n=28) and healthy smokers (n=69). Cilia length was assessed in a total of 228 airway epithelium samples, including 120 LAE samples and 108 SAE samples; a subset of the 228 samples is represented among the 149 samples in this Series.
2014-02-03 | E-GEOD-43939 | biostudies-arrayexpress