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PLAUR polymorphisms and lung function in UK smokers.

Ceri E Stewart1, Ian P Hall, Stuart G Parker

  • 1Division of Therapeutics & Molecular Medicine, Nottingham Respiratory Biomedical Research Unit, University Hospital of Nottingham, Nottingham, UK. ceri.stewart@nottingham.ac.uk

BMC Medical Genetics
|November 3, 2009
PubMed
Summary
This summary is machine-generated.

Genetic variations in the Urokinase Plasminogen Activator Receptor (PLAUR) gene influence lung function in smokers. However, PLAUR single nucleotide polymorphisms (SNPs) are not a major cause of Chronic Obstructive Pulmonary Disease (COPD).

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Area of Science:

  • Genetics
  • Pulmonology
  • Molecular Biology

Background:

  • Urokinase Plasminogen Activator Receptor (PLAUR) was previously identified as an asthma susceptibility gene.
  • This study investigates PLAUR's role in lung function and Chronic Obstructive Pulmonary Disease (COPD) development in smokers.

Purpose of the Study:

  • To determine if PLAUR single nucleotide polymorphisms (SNPs) affect baseline lung function in smokers.
  • To assess the contribution of PLAUR SNPs to COPD susceptibility and severity in smokers.

Main Methods:

  • Genotyped 25 PLAUR SNPs in 992 individuals with smoking history, including COPD cases and controls.
  • Used linear regression to analyze the impact of polymorphisms on lung function (FEV1, FEV1/FVC).
  • Employed logistic regression to compare genotype frequencies between COPD cases and controls, and to assess COPD severity.

Main Results:

  • Five PLAUR SNPs significantly associated with baseline lung function (p < 0.01).
  • Specific SNPs (rs2302524, rs2283628) linked to FEV1, while others (rs740587, rs11668247, rs344779) associated with FEV1/FVC ratio.
  • One SNP (rs740587) showed a protective effect against COPD susceptibility, and another (rs11668247) against COPD severity, particularly in male smokers.

Conclusions:

  • PLAUR gene variations may influence baseline lung function in smokers, consistent with its role in asthma.
  • Case-control analyses suggest PLAUR is not a major determinant of COPD susceptibility in this cohort.
  • PLAUR's known role in plasmin generation and airway remodeling warrants further investigation in respiratory diseases.