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

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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.

Content Provider	Europe PMC
Author	Bi, Hui Wang, Gui Li, Zhiying Zhou, Lin Zhang, Ming Ye, Jiru Wang, Zhigang
Copyright Year	2020
Abstract	BackgroundChronic 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/MethodsHPMECs 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.ResultsOur 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).ConclusionsOur 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.
ISSN	12341010
Journal	Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
Volume Number	26
PubMed Central reference number	PMC7111098
PubMed reference number	32201430
e-ISSN	16433750
DOI	10.12659/msm.920793
Language	English
Publisher	International Scientific Literature, Inc.
Publisher Date	2020-03-23
Access Restriction	Open
Rights License	This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) © Med Sci Monit, 2020
Subject Keyword	Apoptosis Pulmonary Disease, Chronic Obstructive RNA, Long Noncoding
Content Type	Text
Resource Type	Article
Subject	Medicine

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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.

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