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Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis

BACKGROUND: Chronic obstructive pulmonary disease (COPD), a general airway disease, is featured by progressive and chronic immunoreaction in the lung. Increasing evidences have showed that cigarette smoking is the main reason in the COPD progression, and human pulmonary microvascular endothelial cel...

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Autores principales: Bi, Hui, Wang, Gui, Li, Zhiying, Zhou, Lin, Zhang, Ming, Ye, Jiru, Wang, Zhigang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111098/
https://www.ncbi.nlm.nih.gov/pubmed/32201430
http://dx.doi.org/10.12659/MSM.920793
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author Bi, Hui
Wang, Gui
Li, Zhiying
Zhou, Lin
Zhang, Ming
Ye, Jiru
Wang, Zhigang
author_facet Bi, Hui
Wang, Gui
Li, Zhiying
Zhou, Lin
Zhang, Ming
Ye, Jiru
Wang, Zhigang
author_sort Bi, Hui
collection PubMed
description BACKGROUND: Chronic obstructive pulmonary disease (COPD), a general airway disease, is featured by progressive and chronic immunoreaction in the lung. Increasing evidences have showed that cigarette smoking is the main reason in the COPD progression, and human pulmonary microvascular endothelial cell (HPMEC) apoptosis often be observed in COPD, while its pathogenesis is not yet fully described. Upregulation of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was observed in COPD patients, but the specific mechanism of lncRNA MEG3 in COPD remains unknown. The objective of this research was to explore the role of lncRNA MEG3 in cigarette smoke extract (CSE)-induced HPMECs. MATERIAL/METHODS: HPMECs were induced by a series of concentrations of CSE (0%, 0.1%, 1%, and 10%). Then cell apoptosis was analyzed by flow cytometry. Cell apoptosis related proteins were tested using western blot assay. Finally, we applied knockdown and over-expression system to explore the lncRNA MEG3 functions in CSE-induced HPMECs. RESULTS: Our results indicated that various concentrations of CSE (0%, 0.1%, 1%, and 10%) significantly promoted cell apoptosis, augmented caspase-3 activity, upregulated Bax expression, decreased Bcl-2 expression, and enhanced lncRNA MEG3 level in HPMECs. LncRNA MEG3-plasmid transfection resulted in the upregulation of lncRNA MEG3, more apoptotic HPMECs, and higher caspase-3 activity. While lncRNA MEG3 knockdown presented the opposite effects. Further investigation suggested that all the effects of CSE treatment on HPMECs were markedly reversed by lncRNA MEG3-shRNA (short hairpin RNA). CONCLUSIONS: Our study illustrated a protective effect of lncRNA MEG3-shRNA on CSE-induced HPMECs, indicting lncRNA MEG3 can be a new therapeutic approach for COPD treatment.
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spelling pubmed-71110982020-04-03 Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis Bi, Hui Wang, Gui Li, Zhiying Zhou, Lin Zhang, Ming Ye, Jiru Wang, Zhigang Med Sci Monit Lab/In Vitro Research BACKGROUND: Chronic obstructive pulmonary disease (COPD), a general airway disease, is featured by progressive and chronic immunoreaction in the lung. Increasing evidences have showed that cigarette smoking is the main reason in the COPD progression, and human pulmonary microvascular endothelial cell (HPMEC) apoptosis often be observed in COPD, while its pathogenesis is not yet fully described. Upregulation of long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) was observed in COPD patients, but the specific mechanism of lncRNA MEG3 in COPD remains unknown. The objective of this research was to explore the role of lncRNA MEG3 in cigarette smoke extract (CSE)-induced HPMECs. MATERIAL/METHODS: HPMECs were induced by a series of concentrations of CSE (0%, 0.1%, 1%, and 10%). Then cell apoptosis was analyzed by flow cytometry. Cell apoptosis related proteins were tested using western blot assay. Finally, we applied knockdown and over-expression system to explore the lncRNA MEG3 functions in CSE-induced HPMECs. RESULTS: Our results indicated that various concentrations of CSE (0%, 0.1%, 1%, and 10%) significantly promoted cell apoptosis, augmented caspase-3 activity, upregulated Bax expression, decreased Bcl-2 expression, and enhanced lncRNA MEG3 level in HPMECs. LncRNA MEG3-plasmid transfection resulted in the upregulation of lncRNA MEG3, more apoptotic HPMECs, and higher caspase-3 activity. While lncRNA MEG3 knockdown presented the opposite effects. Further investigation suggested that all the effects of CSE treatment on HPMECs were markedly reversed by lncRNA MEG3-shRNA (short hairpin RNA). CONCLUSIONS: Our study illustrated a protective effect of lncRNA MEG3-shRNA on CSE-induced HPMECs, indicting lncRNA MEG3 can be a new therapeutic approach for COPD treatment. International Scientific Literature, Inc. 2020-03-23 /pmc/articles/PMC7111098/ /pubmed/32201430 http://dx.doi.org/10.12659/MSM.920793 Text en © Med Sci Monit, 2020 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Lab/In Vitro Research
Bi, Hui
Wang, Gui
Li, Zhiying
Zhou, Lin
Zhang, Ming
Ye, Jiru
Wang, Zhigang
Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title_full Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title_fullStr Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title_full_unstemmed Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title_short Long Noncoding RNA (lncRNA) Maternally Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis
title_sort long noncoding rna (lncrna) maternally expressed gene 3 (meg3) participates in chronic obstructive pulmonary disease through regulating human pulmonary microvascular endothelial cell apoptosis
topic Lab/In Vitro Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111098/
https://www.ncbi.nlm.nih.gov/pubmed/32201430
http://dx.doi.org/10.12659/MSM.920793
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