Protein expression of PARC in lung tissue and intercostal arteries, according to groups.

<p>Protein expression of PARC in lung tissue and intercostal arteries, according to groups.</p

Colocalization of MIP-4/PARC and alpha smooth muscle actin (αSMA) in arterial tissue.

<p>Representative confocal fluorescence images of human pulmonary muscular (A) and intercostal (E) arteries labeled with antibodies against MIP-4/PARC (red) and αSMA (green). Nuclei were stained in blue. Higher-magnification (x40 oil lents) of representative images shows that MIP-4/PARC (B and F) and αSMA (C and G) were predominantly localized in the media layer of pulmonary and intercostal arteries. Overlay images show, in yellow, a partially colocalization between MIP-4/PARC and αSMA (D and H). Inset in H corresponds to control experiments performed with secondary antibodies alone. Scale bars = 50 μm except for images A and E, where they are 100 μm.</p

PARC gene expression in according to groups.

<p>Data of the PARC mRNA expression (fold change) in lung tissue and intercostal arteries according to groups. No significant differences were found between groups. Data are presented as LSM ± SEM. The reported p-value comes from the pair wise comparison with a general linear model using as covariables: gender, pack-years and the presence of diabetes mellitus.</p

Morphometric parameters of pulmonary muscular arteries and intercostal arteries.

<p>Morphometric parameters of pulmonary muscular arteries and intercostal arteries.</p

Systemic and Pulmonary Vascular Remodelling in Chronic Obstructive Pulmonary Disease

<div><p>Background</p><p>Chronic Obstructive Pulmonary Disease (COPD) is associated with subclinical systemic atherosclerosis and pulmonary vascular remodelling characterized by intimal hyperplasia and luminal narrowing. We aimed to determine differences in the intimal thickening of systemic and pulmonary arteries in COPD subjects and smokers. Secondary aims include comparisons with a non-smokers group; determining the clinical variables associated with systemic and pulmonary intimal thickening, and the correlations between systemic and pulmonary remodelling changes.</p><p>Methods</p><p>All consecutive subjects undergoing lung resection were included and divided into 3 groups: 1) COPD, 2) smokers, and 3) non-smokers. Sections of the 5th intercostal artery and muscular pulmonary arteries were measured by histo-morphometry. Four parameters of intimal thickening were evaluated: 1) percentage of intimal area (%IA), 2) percentage of luminal narrowing, 3) intimal thickness index, and 4) intima-to-media ratio.</p><p>Results</p><p>In the adjusted analysis, the systemic arteries of COPD subjects showed greater intimal thickening (%IA) than those of smokers (15.6±1.5% vs. 14.2±1.6%, p = 0.038). In the pulmonary arteries, significant differences were observed for %IA between the 2 groups (37.3±2.2% vs. 29.3±2.3%, p = 0.016). Among clinical factors, metabolic syndrome, gender and COPD status were associated with the systemic intimal thickening, while only COPD status was associated with pulmonary intimal thickening. A correlation between the %IA of the systemic and pulmonary arteries was observed (Spearman’s rho = 0.46, p = 0.008).</p><p>Conclusions</p><p>Greater intimal thickening in systemic and pulmonary arteries is observed in COPD patients than in smokers. There is a correlation between systemic and pulmonary vascular remodelling in the overall population.</p></div

Additional file 1: of Is the purinergic pathway involved in the pathology of COPD? Decreased lung CD39 expression at initial stages of COPD

Supplementary data. (PDF 360 kb

Linear regression analyses for associations between clinical variables and the intimal thickening (%IA) of systemic arteries in the overall population.

<p>Linear regression analyses for associations between clinical variables and the intimal thickening (%IA) of systemic arteries in the overall population.</p