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Division of Pulmonary and Critical Care Medicine, College of Medicine, Pochon CHA University, Seongnam; National Medical Center; and Asan Medical Center, College of Medicine University of Ulsan, Seoul, Korea
Correspondence and requests for reprints should be addressed to Ji-Hyun Lee, M.D., Ph.D., Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Bundang CHA Hospital, College of Medicine, Pochon CHA University, 351 Yatap-dong, Bundang-gu, Seongnam-si, Kyunggi-do, 463-712 Korea. E-mail: plmjhlee{at}yahoo.co.kr
Bone marrowderived circulating endothelial progenitor cells (cEPCs) are considered to have a key role in the maintenance of vascular integrity and to act as "repair cells" in response to endothelial injury. Some current studies have suggested the role of endothelial cell death in the development of emphysema. Therefore, we hypothesized that smoking-induced endothelial cell injury and death in the absence of sufficient cEPC repair may affect the development of emphysema. Forty-seven patients with stable chronic obstructive pulmonary disease (COPD), 17 smokers with normal lung function, and 13 nonsmokers were included. All patients with COPD had a history of smoking and an irreversible airflow limitation. Patients with COPD were divided into three groups: 17 with chronic bronchitis, 18 with emphysema, and 12 with mixed type. Seven days after plating peripheral blood mononuclear cells (PBMC) to EGM-2 MV Singlequot medium (Cambrex, East Rutherford, NJ), colonies were counted. The number of cEPC colonies was significantly reduced in subjects with emphysema compared to those with chronic bronchitis and nonsmokers. When we divided whole smokers into two groups, emphysema and nonemphysema according to HRCT findings, subjects with emphysema showed lower cEPC colonies than those without emphysema. Also, inverse correlation was noted between cEPC colony count and emphysema degree. Finally, multivariate analysis demonstrated that cEPC was an independent predictor of the presence of emphysema. These findings suggest that cEPCs may be associated with the development of emphysema. However, further studies are needed to determine the role of cEPCs in the pathogenesis of emphysema.
FOOTNOTES
Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.
(Received in original form March 16, 2006; accepted in final form March 20, 2006)
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