Table of Contents Author Guidelines Submit a Manuscript
Canadian Respiratory Journal
Volume 2016 (2016), Article ID 1472823, 10 pages
Clinical Study

Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD

1Department of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8N 3Z5
2Firestone Institute for Respiratory Health, Asthma Research Group, St. Joseph’s Healthcare, 50 Charlton Avenue East, Hamilton, ON, Canada L8N 4A6

Received 27 October 2015; Revised 23 March 2016; Accepted 20 April 2016

Academic Editor: Simon G. Royce

Copyright © 2016 Brittany M. Salter et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic obstructive pulmonary disease (COPD) is characterized by fixed airflow limitation and progressive decline of lung function and punctuated by occasional exacerbations. The disease pathogenesis may involve activation of the bone marrow stimulating mobilization and lung-homing of progenitor cells. We investigated the hypothesis that lower circulating numbers of vascular endothelial progenitor cells (VEPCs) are a consequence of increased lung-sequestration in COPD. Nonatopic, current or ex-smokers with diagnosed COPD and nonatopic, nonsmoking normal controls were enrolled. Blood and induced sputum extracted primitive hemopoietic progenitors (HPCs) and VEPC were enumerated by flow cytometry. Migration and adhesive responses to fibronectin were assessed. In sputum, VEPC numbers were significantly greater in COPD compared to normal controls. In blood, VEPCs were significantly lower in COPD versus normal controls. There were no differences in HPC levels between the two groups in either compartment. Functionally, there was a greater migrational responsiveness of progenitors from COPD subjects to stromal cell-derived factor-1alpha (SDF-1α) compared to normal controls. This was associated with greater numbers of CXCR4+ progenitors in sputum from COPD. Increased migrational responsiveness of progenitor cells may promote lung-homing of VEPC in COPD which may disrupt maintenance and repair of the airways and contribute to COPD disease pathogenesis.