Stromelysin-1 polymorphism as a new potential risk factor in progression of chronic obstructive pulmonary disease

https://doi.org/10.4081/monaldi.2009.371

Authors

  • P. Santus | stefano.centanni@unimi.it Institute of Lung Disease, University of Milan, Respiratory Unit, San Paolo Hospital, Milano, Italy.
  • F. Casanova Institute of Lung Disease, University of Milan, Respiratory Unit, San Paolo Hospital, Milano, Italy.
  • M.L. Biondi Division of Clinical Chemistry and Microbiology, University of Milan, San Paolo Hospital, Milano, Italy.
  • F. Blasi Institute of Lung Disease, University of Milan, IRCCS Policlinico of Milan, Pad. Sacco, Milano, Italy.
  • F. Di Marco Institute of Lung Disease, University of Milan, Respiratory Unit, San Paolo Hospital, Milano, Italy.
  • S. Centanni Institute of Lung Disease, University of Milan, Respiratory Unit, San Paolo Hospital, Milano, Italy.

Abstract

Background. Chronic obstructive lung disease (COPD) is characterised by partially reversible usually progressive airflow limitation caused by inflammation and remodelling. Stromelysin-1 (MMP-3) has regulatory activity on other matrix-metalloproteinases. Altered MMP-3 activity has been described in different diseases. We investigated the role of a promoter MMP-3 polymorphism in determining susceptibility and severity of COPD. Methods. We studied 147 patients with COPD in stable conditions and distinguished two groups based on FEV1 values. In 100 patients functional modifications across a two-year period were noted. 133 healthy subjects were used as controls. Genotyping for the –1171 5A/6A MMP-3 polymorphism was performed using nucleotide sequencing. Results. No difference was noted in the genotype distribution between COPD patients and controls. However, among patients with severe disease 6A/6A genotype and 6A allelic frequency were significantly more represented than among mild-moderate patients (p < 0.05). The 6A/6A genotype was also associated with a higher FEV1 decline over time. Conclusions. Our data suggests that –1171 6A allele does not represent a risk factor for the development of COPD while it is associated with more severe disease and different functional decline. We hypothesise that a disregulation of MMP-3, possibly caused by the –1171 5A/6A polymorphism or other linked variants, may lead to different progression in COPD.

Dimensions

Altmetric

PlumX Metrics

Downloads

Download data is not yet available.

Downloads

Published
2016-01-25
Info
Issue
Section
Original Articles
Keywords:
COPD, candidate genes, Stromelysin-1, Matrix-metalloproteinases, Genotype, Genetic polymorphisms
Statistics
  • Abstract views: 371

  • PDF: 255
How to Cite
Santus, P., F. Casanova, M.L. Biondi, F. Blasi, F. Di Marco, and S. Centanni. 2016. “Stromelysin-1 Polymorphism As a New Potential Risk Factor in Progression of Chronic Obstructive Pulmonary Disease”. Monaldi Archives for Chest Disease 71 (1). https://doi.org/10.4081/monaldi.2009.371.