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Updated: May 6, 2026

Pan-myeloid Differentiation of Human Cord Blood Derived CD34+ Hematopoietic Stem and Progenitor Cells
Published on: August 9, 2019
Circulating hematopoietic progenitor cells are decreased in COPD
William J Janssen1, Zulma X Yunt, Alaina Muldrow
11Division of Pulmonary Medicine, Department of Medicine, National Jewish Health, Denver, CO, USA.
Hematopoietic progenitor cell (HPC) levels are reduced in patients with chronic obstructive pulmonary disease (COPD), particularly those with severe emphysema. This reduction may contribute to COPD pathogenesis by impairing capillary endothelium maintenance.
Area of Science:
- Cardiovascular Biology
- Pulmonary Medicine
- Stem Cell Research
Background:
- Bone marrow progenitor cells are crucial for vascular repair.
- Emphysema is characterized by reduced alveolar capillary density and increased endothelial cell death.
- Circulating progenitor cell levels were hypothesized to be diminished in emphysema patients.
Purpose of the Study:
- Quantify circulating endothelial progenitor cells (EPCs) and hematopoietic progenitor cells (HPCs) in COPD patients.
- Correlate progenitor cell levels with COPD severity and emphysema presence.
- Assess progenitor cell function in COPD.
Main Methods:
- Isolated peripheral blood mononuclear cells from 61 COPD patients and 32 controls.
- Quantified EPCs (CD45dim CD34+) and HPCs (CD45+ CD34+ VEGF-R2+) via multi-parameter flow cytometry.
- Assessed progenitor cell function using cell culture assays and evaluated subjects with spirometry and CT scans.
Main Results:
- HPC levels were significantly lower in COPD subjects compared to controls.
- EPC levels were similar between COPD and control groups.
- Reduced HPC levels correlated with obstruction severity and were lowest in severe emphysema, independent of confounding factors. Endothelial cell colony-forming unit capacity was also reduced in COPD patients.
Conclusions:
- HPC levels are decreased in COPD and linked to emphysema phenotype and obstruction severity.
- Reduced HPCs may impair capillary endothelium maintenance, contributing to COPD pathogenesis.
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