Persistence of circulating endothelial microparticles in COPD despite smoking cessation.

Publication TypeJournal Article
Year of Publication2016
AuthorsStrulovici-Barel Y, Staudt MR, Krause A, Gordon C, Tilley AE, Harvey B-G, Kaner RJ, Hollmann C, Mezey JG, Bitter H, Pillai SG, Hilton H, Wolff G, Stevenson CS, Visvanathan S, Fine JS, Crystal RG
Date Published2016 Dec
KeywordsAdult, Apoptosis, Capillaries, Cell-Derived Microparticles, Endothelial Cells, Endothelium, Vascular, Female, Follow-Up Studies, Humans, Lung, Male, Middle Aged, Pulmonary Disease, Chronic Obstructive, Respiratory Function Tests, Smoking Cessation, Tomography, X-Ray Computed

INTRODUCTION: Increasing evidence links COPD pathogenesis with pulmonary capillary apoptosis. We previously demonstrated that plasma levels of circulating microparticles released from endothelial cells (EMPs) due to apoptosis are elevated in smokers with normal spirometry but low diffusion capacity, that is, with early evidence of lung destruction. We hypothesized that pulmonary capillary apoptosis persists with the development of COPD and assessed its reversibility in healthy smokers and COPD smokers following smoking cessation.

METHODS: Pulmonary function and high-resolution CT (HRCT) were assessed in 28 non-smokers, 61 healthy smokers and 49 COPD smokers; 17 healthy smokers and 18 COPD smokers quit smoking for 12 months following the baseline visit. Total EMP (CD42b(-)CD31(+)), pulmonary capillary EMP (CD42b(-)CD31(+)ACE(+)) and apoptotic EMP (CD42b(-)CD62E(+)/CD42b(-)CD31(+)) levels were quantified by flow cytometry.

RESULTS: Compared with non-smokers, healthy smokers and COPD smokers had elevated levels of circulating EMPs due to active pulmonary capillary endothelial apoptosis. Levels remained elevated over 12 months in healthy smokers and COPD smokers who continued smoking, but returned to non-smoker levels in healthy smokers who quit. In contrast, levels remained significantly abnormal in COPD smokers who quit.

CONCLUSIONS: Pulmonary capillary apoptosis is reversible in healthy smokers who quit, but continues to play a role in COPD pathogenesis in smokers who progressed to airflow obstruction despite smoking cessation.


Alternate JournalThorax
PubMed ID27462120
PubMed Central IDPMC5536242
Grant ListP50 HL084936 / HL / NHLBI NIH HHS / United States
R01 HL107882 / HL / NHLBI NIH HHS / United States
U01 HL121828 / HL / NHLBI NIH HHS / United States
UL1 TR000457 / TR / NCATS NIH HHS / United States