Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD
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 cel...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Canadian Respiratory Journal |
| Online Access: | http://dx.doi.org/10.1155/2016/1472823 |
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| author | Brittany M. Salter Fizza Manzoor Suzanne Beaudin Melanie Kjarsgaard Parameswaran Nair Gail M. Gauvreau Roma Sehmi |
| author_facet | Brittany M. Salter Fizza Manzoor Suzanne Beaudin Melanie Kjarsgaard Parameswaran Nair Gail M. Gauvreau Roma Sehmi |
| author_sort | Brittany M. Salter |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-146490c0d61444f7b85f5a402bc7dcc0 |
| institution | Kabale University |
| issn | 1198-2241 1916-7245 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Canadian Respiratory Journal |
| spelling | doaj-art-146490c0d61444f7b85f5a402bc7dcc02025-02-03T01:26:50ZengWileyCanadian Respiratory Journal1198-22411916-72452016-01-01201610.1155/2016/14728231472823Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPDBrittany M. Salter0Fizza Manzoor1Suzanne Beaudin2Melanie Kjarsgaard3Parameswaran Nair4Gail M. Gauvreau5Roma Sehmi6Department of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaDepartment of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaDepartment of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaFirestone Institute for Respiratory Health, Asthma Research Group, St. Joseph’s Healthcare, 50 Charlton Avenue East, Hamilton, ON, L8N 4A6, CanadaDepartment of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaDepartment of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaDepartment of Medicine, McMaster University, 1280 Main Street West, Hamilton, ON, L8N 3Z5, CanadaChronic 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.http://dx.doi.org/10.1155/2016/1472823 |
| spellingShingle | Brittany M. Salter Fizza Manzoor Suzanne Beaudin Melanie Kjarsgaard Parameswaran Nair Gail M. Gauvreau Roma Sehmi Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD Canadian Respiratory Journal |
| title | Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD |
| title_full | Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD |
| title_fullStr | Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD |
| title_full_unstemmed | Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD |
| title_short | Dysregulation of Vascular Endothelial Progenitor Cells Lung-Homing in Subjects with COPD |
| title_sort | dysregulation of vascular endothelial progenitor cells lung homing in subjects with copd |
| url | http://dx.doi.org/10.1155/2016/1472823 |
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