PECAM EMPs regulate apoptosis in pulmonary microvascular endothelial cells in COPD by activating the Akt signaling pathway
Introduction Endothelial 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)...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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European Publishing
2022-05-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | http://www.tobaccoinduceddiseases.org/PECAM-EMPs-regulate-apoptosis-in-pulmonary-microvascular-nendothelial-cells-in-COPD,146959,0,2.html |
| _version_ | 1811240477749411840 |
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| author | Yuqin Zeng Yiyang Zhao Yan Chen Shan Cai Ping Chen |
| author_facet | Yuqin Zeng Yiyang Zhao Yan Chen Shan Cai Ping Chen |
| author_sort | Yuqin Zeng |
| collection | DOAJ |
| description | Introduction
Endothelial 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.
Methods
We 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.
Results
Unlike 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, in vitro studies showed that the apoptosis rate and expression
of cleaved caspase 3/9 in HPMECs increased in a dose- and time-independent
manner with PECAM EMPs. The expression of phospho-Akt (p-Akt) decreased
in a time-independent manner with PECAM EMPs (p<0.05). Compared with the
control group, the early apoptosis rate of HPMECs was higher, and the expression
of p-Akt was lower in both the PECAM EMP group and EUK-134 + PECAM EMP
group (p<0.05). The apoptosis rate declined markedly, and the expression of p-Akt
was higher in the EUK-134 + PECAM EMP group, compared with the PECAM
EMPs group (p<0.05).
Conclusions
The present results suggest that PECAM EMPs positively regulate
apoptosis in HPMECs in COPD, likely by decreasing Akt phosphorylation and can
be protected by antioxidants. |
| first_indexed | 2024-04-12T13:20:01Z |
| format | Article |
| id | doaj.art-b50590b908ba4ad881b97d88b40eb2a0 |
| institution | Directory Open Access Journal |
| issn | 1617-9625 |
| language | English |
| last_indexed | 2024-04-12T13:20:01Z |
| publishDate | 2022-05-01 |
| publisher | European Publishing |
| record_format | Article |
| series | Tobacco Induced Diseases |
| spelling | doaj.art-b50590b908ba4ad881b97d88b40eb2a02022-12-22T03:31:31ZengEuropean PublishingTobacco Induced Diseases1617-96252022-05-0120May11110.18332/tid/146959146959PECAM EMPs regulate apoptosis in pulmonary microvascular endothelial cells in COPD by activating the Akt signaling pathwayYuqin Zeng0https://orcid.org/0000-0001-6599-3486Yiyang Zhao1Yan Chen2https://orcid.org/0000-0002-7713-6913Shan Cai3https://orcid.org/0000-0003-2296-5228Ping Chen4Department of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of ChinaDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of ChinaDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of ChinaDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of ChinaDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, People’s Republic of ChinaIntroduction Endothelial 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. Methods We 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. Results Unlike 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, in vitro studies showed that the apoptosis rate and expression of cleaved caspase 3/9 in HPMECs increased in a dose- and time-independent manner with PECAM EMPs. The expression of phospho-Akt (p-Akt) decreased in a time-independent manner with PECAM EMPs (p<0.05). Compared with the control group, the early apoptosis rate of HPMECs was higher, and the expression of p-Akt was lower in both the PECAM EMP group and EUK-134 + PECAM EMP group (p<0.05). The apoptosis rate declined markedly, and the expression of p-Akt was higher in the EUK-134 + PECAM EMP group, compared with the PECAM EMPs group (p<0.05). Conclusions The present results suggest that PECAM EMPs positively regulate apoptosis in HPMECs in COPD, likely by decreasing Akt phosphorylation and can be protected by antioxidants.http://www.tobaccoinduceddiseases.org/PECAM-EMPs-regulate-apoptosis-in-pulmonary-microvascular-nendothelial-cells-in-COPD,146959,0,2.htmlpecam empschronic obstructive pulmonary diseaseakt signal pathwayapoptosis |
| spellingShingle | Yuqin Zeng Yiyang Zhao Yan Chen Shan Cai Ping Chen PECAM EMPs regulate apoptosis in pulmonary microvascular endothelial cells in COPD by activating the Akt signaling pathway Tobacco Induced Diseases pecam emps chronic obstructive pulmonary disease akt signal pathway apoptosis |
| title | PECAM EMPs regulate apoptosis in pulmonary microvascular
endothelial cells in COPD by activating the Akt signaling
pathway |
| title_full | PECAM EMPs regulate apoptosis in pulmonary microvascular
endothelial cells in COPD by activating the Akt signaling
pathway |
| title_fullStr | PECAM EMPs regulate apoptosis in pulmonary microvascular
endothelial cells in COPD by activating the Akt signaling
pathway |
| title_full_unstemmed | PECAM EMPs regulate apoptosis in pulmonary microvascular
endothelial cells in COPD by activating the Akt signaling
pathway |
| title_short | PECAM EMPs regulate apoptosis in pulmonary microvascular
endothelial cells in COPD by activating the Akt signaling
pathway |
| title_sort | pecam emps regulate apoptosis in pulmonary microvascular endothelial cells in copd by activating the akt signaling pathway |
| topic | pecam emps chronic obstructive pulmonary disease akt signal pathway apoptosis |
| url | http://www.tobaccoinduceddiseases.org/PECAM-EMPs-regulate-apoptosis-in-pulmonary-microvascular-nendothelial-cells-in-COPD,146959,0,2.html |
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