@article{JTD2665,
author = {Hua Liu and Liang Ding and Yanju Zhang and Songshi Ni},
title = {Circulating endothelial microparticles involved in lung function decline in a rat exposed in cigarette smoke maybe from apoptotic pulmonary capillary endothelial cells},
journal = {Journal of Thoracic Disease},
volume = {6},
number = {6},
year = {2014},
keywords = {},
abstract = {Background: Plasma levels of endothelial microparticles (EMPs), small membrane vesicles, shed from activated or apoptotic endothelial cells are elevated in patients with COPD and in smokers with normal lung function. Whether plasma EMPs levels are elevated in a rat exposed in cigarette smoke, whether the elevated EMPs derived from pulmonary endothelial cell apoptosis, and the relationship between EMP and lung function are obscure.
Methods: All 60 wister rats were divided into six groups, three groups of ten rats were exposed to cigarette smoke of ten non-filter cigarettes per day, 5 days a week, using a standard smoking machine (Beijing BeiLanBo Company, China) for a period of 2, 4 and 6 months (n=10, respectively). Age-matched three control groups were sham-smoked. Pulmonary function parameters, including the ratio of forced expiratory volume in 0.3 second over forced vital capacity (FEV0.3/FVC) and dynamic compliance (Cdyn), were tested at the end of each period (2, 4, 6 months). Blood samples were collected and platelet-free plasma was isolated. Then CD42b–/CD31+ EMPs were analysed by flow cytometry. In parallel, lungs were removed and
Colocalization with terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL), Hoeschts and CD31 was performed to evaluate pulmonary capillaries-specific apoptosis and identify the origins of the EMPs.
Results: At 2, 4 and 6 months, in comparison with control groups, rats in cigarette smoke exposed groups had a significant increase in CD42b–/CD31+ EMPs (P},
issn = {2077-6624}, url = {https://jtd.amegroups.org/article/view/2665}
}