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Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice
Published on: January 16, 2015
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Genes related to emphysema are enriched for ubiquitination pathways
Sergey Stepaniants, I-Ming Wang, Yves Boie
1University of British Columbia Centre for Heart and Lung Innovation, St Paul's Hospital, 1081 Burrard St, Vancouver V6Z 1Y6, BC, Canada. Peter.pare@hli.ubc.ca.
BMC Pulmonary Medicine
|November 30, 2014
Summary
This study reveals that altered protein ubiquitination is a key factor in the development of emphysema, a condition causing airflow limitation in chronic obstructive pulmonary disease (COPD). Understanding these gene expression changes offers new insights into COPD pathogenesis.
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Genetics
Background:
- Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation due to increased small airway resistance and decreased lung elasticity.
- Emphysema, a lesion of lost lung elasticity, and small airway obstruction arise from distinct but converging pathological mechanisms.
- Gene expression patterns may offer more specific insights into COPD phenotypes than traditional lung function comparisons.
Purpose of the Study:
- To investigate the relationship between gene expression and lung tissue phenotypes in smokers.
- To identify specific molecular pathways involved in the pathogenesis of emphysema and small airway obstruction.
Main Methods:
- Measurement of the alveolar surface area to lung volume ratio (SA/V) in lung tissue from 43 smokers.
- Gene expression profiling of samples with significant SA/V differences to identify correlating genes.
- Replication analysis of identified genes in a separate cohort of subjects.
Main Results:
- 181 transcripts showed a significant correlation with SA/V (p < 0.05).
- 30 of these genes were significantly associated with SA/V in the replication cohort (P < 0.05), with consistent directionality in 164/181.
- Pathway analysis identified enrichment of genes involved in protein ubiquitination, confirmed by western blotting in obstructed individuals.
Conclusions:
- Modified protein ubiquitination and degradation pathways are implicated in the pathogenesis of emphysema.
- These findings highlight a novel molecular mechanism contributing to COPD.
- Further research into protein ubiquitination could lead to new therapeutic strategies for COPD.
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