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Lung transcriptomic clock predicts premature aging in cigarette smoke-exposed mice
Mohamed-Amin Choukrallah1, Julia Hoeng2, Manuel C Peitsch2
1Philip Morris International R&D, Quai Jeanrenaud 5, 2003, Neuchâtel, Switzerland. MohamedAmin.Choukrallah@pmi.com.
BMC Genomics
|April 11, 2020
Summary
Lung aging and cigarette smoke (CS) exposure share similar gene expression changes, particularly involving B-cells. A new transcriptomic clock accurately predicts lung biological age and shows CS accelerates aging, which is reversible by quitting or switching to heated tobacco products (HTPs).
Area of Science:
- Pulmonary Medicine
- Genomics
- Toxicology
Background:
- Lung aging involves structural changes like fibrosis and inflammation.
- Chronic cigarette smoke (CS) exposure mimics aging alterations and may accelerate lung aging.
- Both aging and CS exposure induce significant transcriptional changes in lung tissue.
Purpose of the Study:
- To investigate the overlap between age- and CS-associated transcriptomic changes in the lung.
- To develop a transcriptomic clock for predicting biological lung age and the effects of external factors.
- To assess the impact of CS exposure and potential mitigation strategies on lung aging.
Main Methods:
- Comparative transcriptomic analysis of aged and CS-exposed murine lungs.
- Development of a machine learning model (Lasso regression) to predict chronological age from gene expression.
- Validation of the transcriptomic clock using independent datasets and different exposure conditions (fresh air, HTPs, irradiation).
Main Results:
- Significant overlap found between transcriptomic responses to CS and aging in murine lungs.
- Upregulation of immunoglobulin genes observed with age and CS exposure, highlighting B-cell involvement.
- Transcriptomic clock accurately predicted chronological age and identified accelerated lung aging in CS-exposed mice, which was reversible with cessation or HTP use.
Conclusions:
- Aging and CS exposure share common transcriptional patterns in the lung, involving B-cell-related genes.
- Gene expression changes can serve as accurate biomarkers for biological lung age and exposure effects.
- Premature lung aging induced by harmful exposures is potentially reversible.
