Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2021 Jul 28;8(3):382-395.
doi: 10.15326/jcopdf.2021.0211.

Association of Systemic Endothelial-Derived and Platelet-Derived Microparticles With Clinical Outcomes in Chronic Obstructive Pulmonary Disease

Jorge Lascano  1 , Jason Katz  1 , Martin Cearras  2 , Michael Campos  3
Affiliations

Association of Systemic Endothelial-Derived and Platelet-Derived Microparticles With Clinical Outcomes in Chronic Obstructive Pulmonary Disease

Jorge Lascano et al. Chronic Obstr Pulm Dis. .

Abstract

Purpose: Endothelial and platelet microparticles (eMPs and pMPs), markers of cellular activation, dysfunction, or apoptosis, have been associated with multiple cardiovascular conditions. Chronic obstructive pulmonary disease (COPD) is associated with cardiovascular comorbidities and platelet/endothelial dysfunction. We analyzed whether eMPs and pMPs are associated with COPD status and/or severity.

Patients and methods: A total of 58 COPD patients and 19 controls were enrolled and followed for an average of 1.17 years. Characterization of COPD included lung function, Body mass index-airflow Obstruction-Dyspnea-Exercise (BODE) scores, health-related quality of life, exacerbations, comorbidities, and mortality. Plasma collection to measure eMPs and pMPs via flow cytometry was performed at enrollment as well as during acute exacerbation in 17 participants. We measured pMPs (CD31+, CD41+31+, CD 62P+), eMPs (ULEX lectin+, CD51+, CD54+, CD62E+), the apoptotic CD62E+/CD31+ ratio, and Annexin V MP.

Results: As a group, COPD participants had no difference in all MP levels studied compared with controls. No significant correlations with diffusion capacity for carbon monoxide, quality of life, and exacerbation status were found in all MPs studied. However, the eMP ULEX and the pMP CD 62P+ were higher among COPD Global initiative for chronic Obstructive Lung Disease (GOLD) stage 3 patients compared to controls. The CD62E+/CD31+ ratio was lower in controls and GOLD stage 1 COPD participants compared with GOLD stage 2/3 COPD participants, suggesting increased apoptosis. eMP ULEX lectin+ decreased during acute exacerbations and pMP41+31+ significantly increased as BODE score increased.

Conclusions: After adjusting for comorbidities, most eMPs and pMPs studied do not correlate significantly with COPD status or severity.

Keywords: Lung; copd; endothelium; microparticles; platelets.

PubMed Disclaimer

Conflict of interest statement

The authors report no conflicts of interest in this work.

References

    1. Chironi GN,Boulanger CM,Simon A,Dignat-George F,Freyssinet JM,Tedgui A. Endothelial microparticles in diseases. Cell Tissue Res. 2009;335(1):143-151. doi: https://doi.org/10.1007/s00441-008-0710-9 - PubMed
    1. Mackman N. On the trail of microparticles. Circ Res. 2009;104(8):925-927. doi: https://doi.org/10.1161/CIRCRESAHA.109.196840 - PMC - PubMed
    1. Distler JH,Huber LC,Gay S,Distler O,Pisetsky DS. Microparticles as mediators of cellular cross-talk in inflammatory disease. Autoimmunity. 2006;39(8):683-690 . doi: https://doi.org/10.1080/08916930601061538 - PubMed
    1. Horstman LL,Ahn YS. Platelet microparticles: a wide-angle perspective. Crit Rev Oncol Hematol. 1999;30(2):111-142 . doi: https://doi.org/10.1016/S1040-8428(98)00044-4 - PubMed
    1. Soriano AO,Jy W,Chirinos JA,et al. Levels of endothelial and platelet microparticles and their interactions with leukocytes negatively correlate with organ dysfunction and predict mortality in severe sepsis. Crit Care Med. 2005;33(11):2540-2546. doi: https://doi.org/10.1097/01.CCM.0000186414.86162.03 - PubMed