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Related Experiment Video

Updated: Jun 22, 2026

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Automated Measurement of Pulmonary Emphysema and Small Airway Remodeling in Cigarette Smoke-exposed Mice

Published on: January 16, 2015

Accelerated decline in lung function in cigarette smokers is associated with TP53/MDM2 polymorphisms.

Robert J Hancox¹, Richie Poulton, David Welch

¹Dunedin Multidisciplinary Health and Development Research Unit, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.

|June 13, 2009

Summary

The p53 protein helps protect against DNA damage from smoking. Specific gene variants in MDM2 and TP53 are linked to faster lung function decline in smokers.

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Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface

Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface

Published on: February 21, 2011

Area of Science:

Genetics
Pulmonology
Molecular Biology

Background:

p53 protein is known to mediate protective responses against DNA damage in vitro, involving cell-cycle arrest or apoptosis.
These protective mechanisms of p53 have not been definitively demonstrated in human populations.
Cigarette smoke is a significant source of DNA damage in humans, making it a relevant factor for studying p53's role.

Purpose of the Study:

To investigate whether p53-mediated protective responses against DNA damage are demonstrable in humans.
To examine the association between specific genetic polymorphisms in MDM2 and TP53 and lung function in relation to smoking history.
To explore the potential role of p53 in explaining variations in smoking-related lung function impairment.

Main Methods:

A population-based cohort study was conducted.
Lung function was assessed in relation to cumulative smoking history.
Genetic polymorphisms in MDM2 (rs2279744:G/T) and TP53 (rs1042522) were analyzed.

Main Results:

The G-alleles of the MDM2 polymorphism (rs2279744) were associated with higher MDM2 levels, potentially reducing p53 response.
The G-allele of the TP53 polymorphism (rs1042522) encodes arginine and is associated with increased pro-apoptotic activity.
Both the G-alleles in MDM2 and TP53 were significantly associated with an accelerated decline in lung function among smokers.

Conclusions:

The findings support the hypothesis that p53 plays a protective role against DNA damage in humans.
Specific genetic variations in MDM2 and TP53 may influence an individual's susceptibility to smoking-induced lung damage.
This study provides a potential genetic explanation for the observed variability in lung function impairment among cigarette smokers.