miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

Abstract Oxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O2 supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capill...

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Autores principales:	Jizhi Wu, Guangqi Zhang, Hui Xiong, Yuguang Zhang, Gang Ding, Junfeng Ge
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8db28b2838064d11a2aebcbc592b6df8
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spelling	oai:doaj.org-article:8db28b2838064d11a2aebcbc592b6df82021-12-02T17:08:36ZmiR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk10.1038/s41598-021-95712-12045-2322https://doaj.org/article/8db28b2838064d11a2aebcbc592b6df82021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95712-1https://doaj.org/toc/2045-2322Abstract Oxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O2 supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capillaries are often the first to be damaged by hyperoxia, causing many serious consequences. Nevertheless, the molecular mechanism by which hyperoxia injures pulmonary capillary endothelial cells (LMECs) has not been fully elucidated. Therefore, we systematically investigated these issues using next-generation sequencing and functional research techniques by focusing on non-coding RNAs. Our results showed that hyperoxia significantly induced apoptosis and profoundly affected the transcriptome profiles of LMECs. Hyperoxia significantly up-regulated miR-181c-5p expression, while down-regulated the expressions of NCAPG and lncRNA-DLEU2 in LMECs. Moreover, LncRNA-DLEU2 could bind complementarily to miR-181c-5p and acted as a miRNA sponge to block the inhibitory effect of miR-181c-5p on its target gene NCAPG. The down-regulation of lncRNA-DLEU2 induced by hyperoxia abrogated its inhibition of miR-181c-5p function, which together with the hyperoxia-induced upregulation of miR-181c-5p, all these significantly decreased the expression of NCAPG, resulting in apoptosis of LMECs. Our results demonstrated a ceRNA network consisting of lncRNA-DLEU2, miR-181c-5p and NCAPG, which played an important role in hyperoxia-induced apoptosis of vascular endothelial injury. Our findings will contribute to the full understanding of the harmful effects of hyperoxia and to find ways for effectively mitigating its deleterious effects.Jizhi WuGuangqi ZhangHui XiongYuguang ZhangGang DingJunfeng GeNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jizhi Wu Guangqi Zhang Hui Xiong Yuguang Zhang Gang Ding Junfeng Ge miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
description	Abstract Oxygen therapy has been widely used in clinical practice, especially in anesthesia and emergency medicine. However, the risks of hyperoxemia caused by excessive O2 supply have not been sufficiently appreciated. Because nasal inhalation is mostly used for oxygen therapy, the pulmonary capillaries are often the first to be damaged by hyperoxia, causing many serious consequences. Nevertheless, the molecular mechanism by which hyperoxia injures pulmonary capillary endothelial cells (LMECs) has not been fully elucidated. Therefore, we systematically investigated these issues using next-generation sequencing and functional research techniques by focusing on non-coding RNAs. Our results showed that hyperoxia significantly induced apoptosis and profoundly affected the transcriptome profiles of LMECs. Hyperoxia significantly up-regulated miR-181c-5p expression, while down-regulated the expressions of NCAPG and lncRNA-DLEU2 in LMECs. Moreover, LncRNA-DLEU2 could bind complementarily to miR-181c-5p and acted as a miRNA sponge to block the inhibitory effect of miR-181c-5p on its target gene NCAPG. The down-regulation of lncRNA-DLEU2 induced by hyperoxia abrogated its inhibition of miR-181c-5p function, which together with the hyperoxia-induced upregulation of miR-181c-5p, all these significantly decreased the expression of NCAPG, resulting in apoptosis of LMECs. Our results demonstrated a ceRNA network consisting of lncRNA-DLEU2, miR-181c-5p and NCAPG, which played an important role in hyperoxia-induced apoptosis of vascular endothelial injury. Our findings will contribute to the full understanding of the harmful effects of hyperoxia and to find ways for effectively mitigating its deleterious effects.
format	article
author	Jizhi Wu Guangqi Zhang Hui Xiong Yuguang Zhang Gang Ding Junfeng Ge
author_facet	Jizhi Wu Guangqi Zhang Hui Xiong Yuguang Zhang Gang Ding Junfeng Ge
author_sort	Jizhi Wu
title	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
title_short	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
title_full	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
title_fullStr	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
title_full_unstemmed	miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk
title_sort	mir-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via cerna crosstalk
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/8db28b2838064d11a2aebcbc592b6df8
work_keys_str_mv	AT jizhiwu mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk AT guangqizhang mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk AT huixiong mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk AT yuguangzhang mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk AT gangding mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk AT junfengge mir181c5pmediatesapoptosisofvascularendothelialcellsinducedbyhyperoxemiaviacernacrosstalk
_version_	1718381566063804416

miR-181c-5p mediates apoptosis of vascular endothelial cells induced by hyperoxemia via ceRNA crosstalk

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