Endothelial progenitor cells (EPCs) are decreased in cardiac dysfunction morbidity associated with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Therefore, the present study aimed to assess the role of EPCs in AECOPD. Patients with AECOPD (n=27) or stable COPD (n=26) were enrolled. Systemic inflammatory markers (high‑sensitivity C‑reactive protein) were measured. In addition, EPCs were counted, isolated and cultured, and their proliferative, migratory, adhesive and tube‑forming capabilities were determined, in cells from patients with AECOPD and stable COPD. EPC number was lower in patients with AECOPD (5.1±2.6x103/ml) compared with patients with stable COPD (6.0±3.2x103/ml). Migration assay indicated that the early‑EPCs isolated from patients with AECOPD were significantly less mobile than EPCs derived from stable COPD subjects, at a stromal‑cell derived factor‑1α concentration of 100 ng/ml (3,550/30,000 vs. 7,853/30,000, P<0.05). C‑X‑C chemokine receptor‑4 positivity was significantly reduced in AECOPD patients (16.1±9.9 vs. 56.33±6.3%, P<0.05). Furthermore, fewer early‑EPC clusters were formed by EPCs derived from AECOPD, compared with those derived from stable COPD (8.2±0.86 vs. 14.4±1.36, P=0.027). Stable COPD late‑EPCs were markedly deficient in intact tubule formation, however AECOPD late‑EPCs formed no tubules. The number of AECOPD‑ and stable COPD‑derived late‑EPCs adhering to Matrigel‑induced tubules was 36.8±1.85 and 20.6±1.36 (P<0.05) respectively, and the cluster of differentiation 31 positivity in late‑EPCs was 79.69±1.3 and 29.1±2.47%, in AECOPD and stable COPD patients, respectively (P<0.001). The findings demonstrated that early‑EPCs are decreased and dysfunctional in AECOPD patients, which may contribute to the altered vascular endothelium in this patient population.

Related Articles