Endothelial progenitor cell dysfunction in acute exacerbation of chronic obstructive pulmonary disease.
Endothelial progenitor cell dysfunction in acute exacerbation of chronic obstructive pulmonary disease.
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慢性阻塞性肺疾病急性加重时的内皮祖细胞功能障碍
DOI：
10.3892/mmr.2017.7260
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发表时间：
2017-10
影响因子：
3.4
通讯作者：
Xie C
中科院分区：
文献类型：
--
作者：
Liu X;Liu Y;Huang X;Lin G;Xie C
内皮祖细胞(EPC)在慢性阻塞性肺疾病急性加重(AECOPD)相关的心功能障碍发病率方面减少。因此，本研究旨在评估内皮祖细胞在AECOPD中的作用。纳入AECOPD(n=27)和稳定期COPD(n=26)患者。检测全身炎症标志物(高敏C反应蛋白)。此外，在AECOPD和稳定期COPD患者的细胞中，计数、分离和培养内皮祖细胞，并测定其增殖、迁移、黏附和成管能力。AECOPD组EPC数(5.1±2.6×103/ml)明显低于稳定期COPD组(6.0±3.2×103/ml)。迁移分析显示，在基质细胞衍生因子-1α浓度为100 ng/ml时，从急性慢阻肺患者分离的早期内皮祖细胞的流动性明显低于来自稳定期患者的内皮祖细胞(3,550/30,000对7,853/30,000，P<；0.05)。AECOPD患者C-X-C趋化因子受体4阳性率显著降低(16.1±9.9比56.33±6.3%，P<0.05)。此外，来自AECOPD的EPC形成的早期EPC簇少于来自稳定期COPD的EPC(8.2±0.86vs.14.4±1.36，P=0.027)。稳定的COPD晚期内皮祖细胞明显缺乏完整的小管形成，而AECOPD晚期内皮祖细胞没有形成小管。AECOPD组和稳定期COPD组晚期EPC黏附于Matrigel诱导的小管的数量分别为36.80±1.85和20.6±1.36(P<；0.001)，晚期EPC的分化簇数分别为79.69±1.30和29.1±2.47%。研究结果表明，AECOPD患者早期内皮祖细胞减少和功能紊乱，这可能是该患者群体血管内皮细胞改变的原因之一。
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±2.6×103/ml) compared with patients with stable COPD (6.0±3.2×103/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.
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影响因子：
9.6
作者：
Lee, Hwa Mu;Lee, Janet;Wong, Nathan D.
通讯作者：
Wong, Nathan D.
影响因子：
2.6
作者：
Liu, Yangli;Liu, Xiaoran;Xie, Canmao
通讯作者：
Xie, Canmao
影响因子：
9.6
作者：
Sidney, S;Sorel, M;Eisner, MD
通讯作者：
Eisner, MD
DOI：
10.1513/pats.200405-033ms
发表时间：
2005-01-01
期刊：
Proceedings of the American Thoracic Society
影响因子：
--
作者：
Voelkel, Norbert;Taraseviciene-Stewart, Laima
通讯作者：
Taraseviciene-Stewart, Laima
影响因子：
9.6
作者：
Niewoehner, Dennis E.;Lokhnygina, Yuliya;Kesten, Steven
通讯作者：
Kesten, Steven