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The role of matrix metalloproteinase polymorphisms in the rate of decline in lung function

Ladina Joos1, Jian-Qing He, Megan B Shepherdson

  • 1University of British Columbia McDonald Research Laboratories/iCAPTURE Center, St Paul's Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada.

Human Molecular Genetics
|March 5, 2002
PubMed

Insights

Genetic variations in matrix metalloproteinase (MMP) genes, specifically MMP1 and MMP12, are linked to faster lung function decline in smokers. These MMP gene polymorphisms may contribute to smoking-related lung injury in chronic obstructive lung disease.

Area of Science:

  • Genetics
  • Pulmonology
  • Biochemistry

Background:

  • Matrix metalloproteinases (MMPs) are key enzymes in tissue remodeling.
  • MMP1, MMP9, and MMP12 are implicated in emphysema development.
  • Gene polymorphisms can affect MMPs' transcriptional activity.

Purpose of the Study:

  • To investigate the role of MMP gene polymorphisms in chronic obstructive lung disease (COPD).
  • To determine the prevalence of MMP polymorphisms in smokers with varying rates of lung function decline.

Main Methods:

  • Studied 590 smokers from the Lung Health Study with fast and slow lung function decline rates.
  • Analyzed five MMP gene polymorphisms, including MMP1 G-1607GG and MMP12 Asn357Ser.
  • Used statistical analysis to associate polymorphisms and haplotypes with lung function decline.

Main Results:

  • The MMP1 G-1607GG polymorphism was associated with a faster rate of lung function decline (P=0.02).
  • Haplotypes of MMP1 G-1607GG and MMP12 Asn357Ser polymorphisms showed a significant association with lung function decline (P=0.0007).
  • MMP9 polymorphisms were not associated with lung function decline.

Conclusions:

  • MMP1 and MMP12 gene polymorphisms, but not MMP9, are associated with smoking-related lung injury.
  • These polymorphisms may be causative or in linkage disequilibrium with causative factors in COPD development.
  • Further research into MMP gene variations could inform COPD prevention and treatment strategies.

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