Doyle Margaret F, Tracy Russell P, Parikh Megha A, Hoffman Eric A, Shimbo Daichi, Austin John H M, Smith Benjamin M, Hueper Katja, Vogel-Claussen Jens, Lima Joao, Gomes Antoinette, Watson Karol, Kawut Steven, Barr R Graham
Department of Pathology and Laboratory Medicine, University of Vermont, Burlington, Vermont, United States of America.
Department of Medicine, Columbia University, New York, New York, United States of America.
PLoS One. 2017 Mar 14;12(3):e0173446. doi: 10.1371/journal.pone.0173446. eCollection 2017.
Endothelial injury is implicated in the pathogenesis of COPD and emphysema; however the role of endothelial progenitor cells (EPCs), a marker of endothelial cell repair, and circulating endothelial cells (CECs), a marker of endothelial cell injury, in COPD and its subphenotypes is unresolved. We hypothesized that endothelial progenitor cell populations would be decreased in COPD and emphysema and that circulating endothelial cells would be increased. Associations with other subphenotypes were examined. The Multi-Ethnic Study of Atherosclerosis COPD Study recruited smokers with COPD and controls age 50-79 years without clinical cardiovascular disease. Endothelial progenitor cell populations (CD34+KDR+ and CD34+KDR+CD133+ cells) and circulating endothelial cells (CD45dimCD31+CD146+CD133-) were measured by flow cytometry. COPD was defined by standard spirometric criteria. Emphysema was assessed qualitatively and quantitatively on CT. Full pulmonary function testing and expiratory CTs were measured in a subset. Among 257 participants, both endothelial progenitor cell populations, and particularly CD34+KDR+ endothelial progenitor cells, were reduced in COPD. The CD34+KDR+CD133+ endothelial progenitor cells were associated inversely with emphysema extent. Both endothelial progenitor cell populations were associated inversely with extent of panlobular emphysema and positively with diffusing capacity. Circulating endothelial cells were not significantly altered in COPD but were inversely associated with pulmonary microvascular blood flow on MRI. There was no consistent association of endothelial progenitor cells or circulating endothelial cells with measures of gas trapping. These data provide evidence that endothelial repair is impaired in COPD and suggest that this pathological process is specific to emphysema.
内皮损伤与慢性阻塞性肺疾病(COPD)和肺气肿的发病机制有关;然而,内皮祖细胞(EPCs,内皮细胞修复的标志物)和循环内皮细胞(CECs,内皮细胞损伤的标志物)在COPD及其亚表型中的作用尚未明确。我们假设COPD和肺气肿患者的内皮祖细胞数量会减少,而循环内皮细胞数量会增加。我们还研究了它们与其他亚表型的关联。动脉粥样硬化多民族COPD研究招募了患有COPD的吸烟者和年龄在50 - 79岁且无临床心血管疾病的对照组。通过流式细胞术测量内皮祖细胞数量(CD34 + KDR +和CD34 + KDR + CD133 +细胞)和循环内皮细胞(CD45dimCD31 + CD146 + CD133 -)。COPD由标准肺量计标准定义。通过CT对肺气肿进行定性和定量评估。在一个亚组中进行了全肺功能测试和呼气CT测量。在257名参与者中,COPD患者的内皮祖细胞数量,尤其是CD34 + KDR +内皮祖细胞数量减少。CD34 + KDR + CD133 +内皮祖细胞与肺气肿程度呈负相关。两种内皮祖细胞数量均与全小叶肺气肿程度呈负相关,与弥散能力呈正相关。COPD患者的循环内皮细胞没有显著改变,但与MRI上的肺微血管血流呈负相关。内皮祖细胞或循环内皮细胞与气体潴留指标之间没有一致的关联。这些数据提供了证据,表明COPD患者的内皮修复受损,并表明这种病理过程是肺气肿所特有的。