Increased circulating endothelial microparticles in COPD patients: a potential biomarker for COPD exacerbation susceptibility.

نویسندگان

  • Toru Takahashi
  • Seiichi Kobayashi
  • Naoya Fujino
  • Takaya Suzuki
  • Chiharu Ota
  • Mei He
  • Mitsuhiro Yamada
  • Satoshi Suzuki
  • Masaru Yanai
  • Shin Kurosawa
  • Mutsuo Yamaya
  • Hiroshi Kubo
چکیده

RATIONALE The influence of COPD exacerbation on the endothelium is not completely understood. Circulating endothelial microparticles (EMPs) are membrane vesicles in circulating blood that are shed by activated or apoptotic endothelial cells. OBJECTIVE To compare EMP numbers in stable COPD patients with those during and after exacerbation. METHODS We examined the EMP numbers in 80 stable COPD patients, 27 patients with exacerbated COPD, and 20 healthy non-COPD volunteers. EMPs were defined as CD144+ MPs (VE-cadherin EMPs), CD31+/CD41- MPs (PECAM EMPs), CD146 MPs (MCAM EMPs) and CD62E+ EMPs (E-selectin EMPs) as analysed by FACS. Von Willebrand factor (vWF) expression was utilised to identify the origins of the EMPs. RESULTS VE-cadherin, PECAM and E-selectin EMP numbers were significantly higher in the stable COPD patients than in the non-COPD volunteers, and they were significantly higher in the patients with exacerbated COPD than in the stable COPD patients. The majority of these increased EMPs were vWF-negative, indicating a pulmonary capillary origin. Baseline E-selectin EMP levels were significantly higher in COPD patients who experienced frequent exacerbations than in those who did not have frequent exacerbations (p<0.001). Twenty-eight days after the onset of exacerbation, E-selectin EMP levels returned to those observed in stable COPD patients, whereas PECAM EMP levels remained high. MCAM EMP numbers were not elevated in stable or exacerbated-COPD patients. CONCLUSIONS Endothelial damage, mainly in pulmonary capillaries, occurs during exacerbation and continues even after clinical symptoms disappear. Higher baseline E-selectin EMP levels may indicate COPD patients who are susceptible to exacerbation.

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عنوان ژورنال:
  • Thorax

دوره 67 12  شماره 

صفحات  -

تاریخ انتشار 2012