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TRANSLATIONAL AND CLINICAL RESEARCH |
aDepartment of Clinical and Experimental Medicine, Division of Metabolic Diseases,
bDepartment of Cardiac, Thoracic and Vascular Sciences, Thoracic Surgery Branch,
dDepartment of Clinical and Experimental Medicine, Clinical Immunology and Hematology, University of Padova School of Medicine, Padova, Italy;
cUnità Locale Socio-Sanitaria 17 Veneto Region (Italy), Social Pneumology Service, Italy
Key Words. Endothelial progenitor cells • Stem cells • Endothelial dysfunction • Pulmonary disease
Correspondence: Gian Paolo Fadini, M.D.,Dipartimento di Medicina Clinica e Sperimentale, Divisione di Malattie del Metabolismo, Università degli Studi di Padova, Via Giustiniani 2, 35128 Padova, Italy. Telephone: 0039-333-5682517 Fax: 0039-049-8754179 email: gianpaolofadini{at}hotmail.com
Received September 8, 2005;
accepted for publication March 27, 2006.
First published online in STEM CELLS EXPRESS April 6, 2006.
Patients with chronic severe lung disease are prone to develop pulmonary vascular remodeling, possibly through pulmonary endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are involved in maintenance of endothelial homeostasis. The aim of this study was to assess whether obstructive and restrictive lung diseases are associated with modification of EPC number in peripheral blood. The study was cross-sectional and involved patients with obstructive (n = 15) and restrictive (n = 15) lung disease on oxygen therapy and 15 control subjects. Circulating EPCs were defined by the surface expression of CD34, CD133, and kinase-insert domain receptor. Results from spirometric tests, blood gas analyses, and blood cell counts have been related to EPC numbers. Patients with chronic hypoxia and severe lung disease showed lower levels of all progenitors than do control subjects. A consensual further reduction of EPC was found in restrictive patients in comparison with obstructive patients. Among restrictive patients, EPC reduction was related to reduced lung volumes and impaired alveolo-arterial diffusion, whereas progenitor cell levels were directly related to erythrocyte number. Considering obstructive patients, significant correlations were found between progenitor cell levels and bronchial obstruction and between progenitor cell levels and arterial oxygen tension. These findings demonstrate a reduction of EPCs in patients with chronic lung disease and long-lasting hypoxia. This alteration was more evident in restrictive patients and correlated to disease severity. Depletion of circulating EPCs may be involved in altered endothelial homeostasis of pulmonary circulation in these disorders.
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