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Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22

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资源类型：
Pubmed体系：
作者：
Song Yaxian[1] * ; Yang Lixia[2,*1] ; Guo Ruiwei[2] ; Lu Nihong[1] ; Shi Yankun[2] ; Wang Xianmei[2] ;
机构： [1]Department of Postgraduate, Kunming Medical University, Yunnan, 650500, China [2]Department of Cardiology, The 920th Hospital of Joint Logistics Support Force of the Chinese People's Liberation Army, Yunnan, China
出处：
DOI： 10.1016/j.bbrc.2018.12.139
ISSN：

关键词： MALAT1 Pyroptosis Atherosclerosis Endothelial cells miR-22 NLRP3

摘要：
Cell death and inflammation play critical roles in atherosclerosis. Pyroptosis, a novel proinflammatory programmed cell death process, participates in atherosclerosis pathogenesis. Recently, MALAT1 was identified as a pyroptosis-related long noncoding RNA (lncRNA). Here, we investigated the potential role and underlying mechanism of lncRNA MALAT1 in endothelial cells pyroptosis. We first established an endothelial cell pyroptosis model by stimulating EA.hy926 human endothelial cells (EA.hy926 cells) with high glucose. Then, we investigated lncRNA MALAT1 expression and found that it was upregulated in high glucose-treated EA.hy926 cells. Furthermore, lncRNA MALAT1 knockdown significantly inhibited high glucose-induced pyroptosis in EA.hy926 cells, which may critically influence atherosclerosis. Moreover, miR-22 was a target of lncRNA MALAT1 and was negatively correlated with lncRNA MALAT1. NLRP3 expression was significantly suppressed by transfection with a MALAT1-targeting antisense oligonucleotide (ASO). Ultimately, miR-22 overexpression abrogated the effect of MALAT1 on high glucose-induced EA.hy926 cells pyroptosis. Together, our results suggest that lncRNA MALAT1 promotes high glucose-induced pyroptosis of endothelial cells partly by affecting NLRP3 expression through competitively binding miR-22. Our findings indicate a new regulatory mechanism for endothelial cells pyroptosis under high-glucose stress, providing a novel therapeutic target for atherosclerosis.Copyright © 2018 Elsevier Inc. All rights reserved.

语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2019]版：
大类 | 3 区 生物
小类 | 3 区 生物物理 4 区 生化与分子生物学
最新[2023]版：
大类 | 3 区 生物学
小类 | 3 区 生物物理 4 区 生化与分子生物学
第一作者：
第一作者机构： [1]Department of Postgraduate, Kunming Medical University, Yunnan, 650500, China
通讯作者：
通讯机构： [2]Department of Cardiology, The 920th Hospital of Joint Logistics Support Force of the Chinese People's Liberation Army, Yunnan, China [*1]Department of Cardiology, The 920th Hospital of Joint Logistics Support Force of the Chinese People's Liberation Army, Yunnan, 650032, China.
推荐引用方式(GB/T 7714)：
Song Yaxian,Yang Lixia,Guo Ruiwei,et al.Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22[J].Biochemical and biophysical research communications.2019,509(2):359-366.doi:10.1016/j.bbrc.2018.12.139.
APA：
Song Yaxian,Yang Lixia,Guo Ruiwei,Lu Nihong,Shi Yankun&Wang Xianmei.(2019).Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22.Biochemical and biophysical research communications,509,(2)
MLA：
Song Yaxian,et al."Long noncoding RNA MALAT1 promotes high glucose-induced human endothelial cells pyroptosis by affecting NLRP3 expression through competitively binding miR-22".Biochemical and biophysical research communications 509..2(2019):359-366

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