Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

MicroRNA expression from bronchial epithelial cell samples of current and never smokers.

ABSTRACT: MicroRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy from healthy current and never smoker volunteers in order to determine the effect of cigarette smoke exposure on airway epithelial microRNA expression Keywords: Global microRNA expression profiling Bronchial epithelial cells were collected from current and never smokers via bronchoscopy. Low molecular weight RNA ( < 200 nucleotides) was isolated and hybridized to Invitrogen NCode microRNA microarrays to determine which microRNAs detected in bronchial epithelial cells were differentially expressed in the airways of smokers.

ORGANISM(S): Homo sapiens

SUBMITTER: Sriram Sridhar

PROVIDER: E-GEOD-14634 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium.

Schembri Frank F Sridhar Sriram S Perdomo Catalina C Gustafson Adam M AM Zhang Xiaoling X Ergun Ayla A Lu Jining J Liu Gang G Zhang Xiaohui X Bowers Jessica J Vaziri Cyrus C Ott Kristen K Sensinger Kelly K Collins James J JJ Brody Jerome S JS Getts Robert R Lenburg Marc E ME Spira Avrum A

Proceedings of the National Academy of Sciences of the United States of America 20090123 7

We have shown that smoking impacts bronchial airway gene expression and that heterogeneity in this response associates with smoking-related disease risk. In this study, we sought to determine whether microRNAs (miRNAs) play a role in regulating the airway gene expression response to smoking. We examined whole-genome miRNA and mRNA expression in bronchial airway epithelium from current and never smokers (n = 20) and found 28 miRNAs to be differentially expressed (P < 0.05) with the majority being ...[more]

PMID: 19168627

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Project description:Background: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characterized by varying degrees of emphysematous lung destruction and small airway disease, each with distinct effects on clinical outcomes. There is little known about how microRNAs contribute specifically to the emphysema phenotype. We examined how microRNA expression is altered with regional emphysema severity within the lung and how these microRNAs regulate disease-associated gene-expression networks. Results: We profiled microRNAs in different regions in the lung with varying degrees of emphysema from 6 smokers with COPD and 2 controls (8 regions x 8 lungs = 64 samples). 63 microRNAs (p<0.05) were altered with regional emphysema severity as quantified by mean linear intercept (Lm). MicroRNA and gene expression data were then integrated in the same samples. A subset of microRNAs, including miR-638, miR-30c, and miR-181d, correlated with many of their predicted gene targets, suggesting a role in regulating the gene networks that underlie emphysematous lung destruction. Modulating miR-638 expression in primary human lung fibroblasts recapitulated the alterations in its targeted gene-expression network associated with emphysema progression. Pathway analysis revealed that genes involved in oxidative stress and accelerated aging were affected by miR-638 knock-down in fibroblasts. Many miR-638 gene targets in these pathways were amongst those negatively correlated with miR-638 expression in emphysematous lung tissue. Conclusions: Our findings demonstrate that microRNAs are altered with regional emphysema severity and modulate disease-associated gene expression networks. Furthermore, miR-638 may regulate gene expression associated with the oxidative stress response and aging in emphysematous lung tissue and fibroblasts. Paired samples were obtained from 8 regions at regular intervals between the apex and base of each explanted lung from six patients with severe COPD and two donors. The degree of emphysematous destruction was quantified in one sample from each region by mean linear intercept (Lm), while microRNA expression was profiled in the adjacent sample from the same region using the NCode Version 3 microRNA microarrays (Invitrogen, Carlsbad, CA). After quality control 60 samples were used for the analysis.

Dataset Information

MicroRNA expression from bronchial epithelial cell samples of current and never smokers.

Publications

MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium.

Similar Datasets

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