Transcriptomics,Genomics

Dataset Information

33

Transcriptomic analysis of lung tissue from cigarette smoke induced emphysema murine models and human COPD show shared and distinct pathways


ABSTRACT: Although cigarette smoke (CS) is the primary risk factor for COPD, the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6J, NZW/LacJ) and two genetic models with mutations in COPD GWAS genes (HHIP, FAM13A) after 6 months of chronic CS exposure and compared the results to human COPD lung tissues. We identified gene response patterns that correlate with severity of emphysema in mouse and human lungs. Xenobiotic metabolism and Nrf2-mediated oxidative stress response were commonly regulated molecular response patterns across C57BL/6J, Hhip +/- and Fam13a -/- murine models upon chronic CS exposure and human COPD subjects. The CS resistant Fam13a -/- mouse and NZW/LacJ strain revealed an opposite pattern of gene expression response, suggesting distinct molecular pathways for resistance against emphysema. There were few genes commonly modulated between mouse and humans. Our study suggests gene expression responses to CS may be largely species and model dependent, yet shared pathways could provide biologically significant insights underlying individual susceptibility to CS Overall design: Total RNA was obtained from the lung tissue of C57BL/6J wild type, Hhip+/- , Fam13a -/- and NZW/LacJ exposed to cigarette smoke (CS) or filtered air (air) for 6 months and gene expression profiling was performed on murine lungs.

INSTRUMENT(S): Illumina MouseRef-8 v2.0 expression beadchip

SUBMITTER: Jeong Hyun Yun  

PROVIDER: GSE87292 | GEO | 2017-09-05

SECONDARY ACCESSION(S): PRJNA344029

REPOSITORIES: GEO

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Publications

Transcriptomic Analysis of Lung Tissue from Cigarette Smoke-Induced Emphysema Murine Models and Human Chronic Obstructive Pulmonary Disease Show Shared and Distinct Pathways.

Yun Jeong H JH   Morrow Jarrett J   Owen Caroline A CA   Qiu Weiliang W   Glass Kimberly K   Lao Taotao T   Jiang Zhiqiang Z   Perrella Mark A MA   Silverman Edwin K EK   Zhou Xiaobo X   Hersh Craig P CP  

American journal of respiratory cell and molecular biology 20170701 1


Although cigarette smoke (CS) is the primary risk factor for chronic obstructive pulmonary disease (COPD), the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6 and NZW/LacJ) and two genetic models with mutations in COPD genome-wide association study genes (HHIP and FAM13A) after 6 months of chronic CS exposure and compared  ...[more]

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