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This Article Full Text (PDF) Free Supplemental data All Versions of this Article: chest.06-2819v1 132/6/1733    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Baraldo, S. Articles by Saetta, M. Search for Related Content PubMed PubMed Citation Articles by Baraldo, S. Articles by Saetta, M. Related Content Related Editorial

Matrix Metalloproteinase-2 protein in lung periphery is related to COPD progression.

¹University of Padova, Department of Cardio-thoracic and Vascular Sciences, Padova, Italy ²University of Padova, Department of Experimental Biomedical Sciences, Padova, Italy ³University of Padova, Department of Environmental Medicine and Public Health, Padova, Italy ⁴University of Ferrara, Department of Clinical and Experimental Medicine, Ferrara, Italy ⁵National Institute of Research, Institute of Physiology, Pisa, Italy ⁶University of Modena and Reggio Emilia, Department of Oncology, Haematology and Respiratory Disease, Modena, Italy

marina.saetta{at}unipd.it

Abstract

BackgroundThere is increasing evidence that metalloproteinases (MMPs) may contribute to the pathogenesis of COPD, but their role in humans is not completely understood. We performed this study to quantify the expression of MMP-2 in a population of COPD patients at different stages of severity.

MethodsWe collected surgical specimens from 46 subjects: 10 smokers with severe COPD (GOLD III-IV), 13 smokers with mild/moderate COPD (GOLD I-II), 12 control smokers and 11 nonsmoking controls. We quantified MMP-2 expression in alveolar macrophages, alveolar walls, peripheral airways and pulmonary arterioles by immunohistochemistry, as well as the total number of alveolar macrophages.

ResultsIn all compartments MMP-2 expression was increased in both smokers with severe COPD and smokers with mild/moderate COPD compared to control smokers and nonsmokers (p<0.05 for all comparisons). Only in the alveolar compartment was MMP-2 expression increased in smokers with severe COPD compared to smokers with mild/moderate COPD (p=0.002). Moreover, MMP-2 expression was inversely related to values of FEV₁/FVC% (p<0.0001; r=-0.71) and PaO₂ mmHg (p=0.005; r=-0.49), and positively related to values of emphysema score (p=0.01; r=0.65) and residual volume (p=0.04; r=0.49). A stepwise increase in total number of alveolar macrophages was observed in the 4 groups of subjects examined, with the highest value in severe COPD.

ConclusionThis study shows that MMP-2 expression in lung periphery progressively increases as lung function worsens and degree of emphysema increases. These results suggest that MMP-2 may be a key mediator of the mechanisms leading to lung tissue remodelling and inflammation in severe COPD.

Key Words: emphysema • extracellular matrix • airflow limitation • cigarette smoking • inflammation

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Proteases in COPD: A Critical Pathway to Injury

Gerard M. Turino
Chest 2007 132: 1724-1725. [Full Text] [PDF]

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				G. M. Turino Proteases in COPD: A Critical Pathway to Injury Chest, December 1, 2007; 132(6): 1724 - 1725. [Full Text] [PDF]