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23 March 2020 : Laboratory Research  

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

Hui Bi1ABCDEFG*, Gui Wang2BCDF, Zhiying Li1BCD, Lin Zhou1BCD, Ming Zhang1BCD, Jiru Ye1BF, Zhigang Wang1BF

DOI: 10.12659/MSM.920793

Med Sci Monit 2020; 26:e920793


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 AND 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.

Keywords: Pulmonary Disease, Chronic Obstructive, endothelial cells, Gene Expression Regulation, Gene Expression Regulation, Developmental, Smoke, Tobacco


Med Sci Monit 2020; 26:e927410     https://medscimonit.com/abstract/index/idArt/927410

Figure 3 was incorrectly published in the article titled Long Noncoding RNA (lncRNA) Maternally-Expressed Gene 3 (MEG3) Participates in Chronic Obstructive Pulmonary Disease Through Regulating Human Pulmonary Microvascular Endothelial Cell Apoptosis; PMID: 32201430; PMCID: PMC7111098; DOI: 10.12659/MSM.920793. The correct Figure 3 is as follows.
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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750