ArticleTobacco induced diseases2022
PECAM EMPs regulate apoptosis in pulmonary microvascular endothelial cells in COPD by activating the Akt signaling pathway.
Article in Tobacco induced diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Endothelial dysfunction in chronic obstructive pulmonary disease: an update on mechanisms, assessment tools and treatment strategies.Frontiers in medicine · 2025Review
- Review
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionEndothelial microparticles (EMPs) are partly associated with the progress of chronic obstructive pulmonary disease (COPD). We sought to measure the levels of EMPs in COPD patients and in human pulmonary microvascular endothelial cells (HPMECs) exposed to cigarette smoking extract (CSE) to elucidate the potential mechanisms of their action.
methodsWe obtained prospectively blood EMPs from 30 stable COPD patients and 20 non-COPD volunteers. EMP subpopulations were determined by flow cytometry in platelet-free plasma according to the expression of membrane specific antigens. Cell growth, proliferation, apoptosis and the expression of protein kinase B (Akt) in HPMECs after exposure to PECAM EMPs were assessed. After intervention with an antioxidant (Eukarion-134, EUK-134), apoptosis and the expression of Akt in HPMECs were also measured.
resultsUnlike those of MCAM EMPs, VE-cadherin, PECAM and E-selectin EMP values were significantly higher in the stable COPD patients than in the non-COPD volunteers (p<0.05). Only PECAM EMPs were higher in HPMECs exposed to CSE (p<0.05). Further,
conclusionsThe present results suggest that PECAM EMPs positively regulate apoptosis in HPMECs in COPD, likely by decreasing Akt phosphorylation and can be protected by antioxidants.
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