The lncRNA MALAT1 protects the endothelium against ox-LDL-induced dysfunction via upregulating the expression of the miR-22-3p target genes CXCR2 and AKT

被引:118
|
作者
Tang, Yong [1 ]
Jin, Xian [1 ,2 ]
Xiang, Yin [1 ]
Chen, Yu [3 ]
Shen, Cheng-xing [1 ]
Zhang, Ya-chen [1 ]
Li, Yi-gang [1 ]
机构
[1] Shanghai Jiao Tong Univ, Xinhua Hosp, Dept Cardiol, Sch Med, Shanghai 200092, Peoples R China
[2] Cent Hosp Minhang Dist, Dept Cardiol, Shanghai, Peoples R China
[3] Shanghai Jiao Tong Univ, Peoples Hosp 9, Dept Cardiol, Sch Med, Shanghai 200092, Peoples R China
基金
中国国家自然科学基金;
关键词
CXCR2; miRNA-22-3p; MALAT1; Endothelial cells; ox-LDL; NONCODING RNA MALAT1; LOW-DENSITY-LIPOPROTEIN; COLORECTAL-CANCER CELLS; PATHOGENIC ROLE; ATHEROSCLEROSIS; PROLIFERATION; APOPTOSIS; CARCINOMA; MICRORNAS; RECEPTOR;
D O I
10.1016/j.febslet.2015.08.046
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
CXCR2 plays a key role in protecting the integrity of the endothelium. Emerging evidence has demonstrated that the long ncRNAs (IncRNA) Human metastasis associated lung adenocarcinoma transcript 1 (MALAT1) participates in the regulation of the pathophysiological processes. However, whether there is crosstalk between CXCR2 and MALAT1 remains unknown. In this study, we demonstrated that MALAT1 was upregulated in patients with unstable angina. MALAT1 silencing significantly downregulated the expression of the miR-22-3p target gene CXCR2 via reversing the effect of the miR-22-3p, resulting in the aggravation of Oxidized low-density lipoprotein (ox-LDL)-induced endothelial injury; this process was associated with the AICT pathway. Thus, MALAT1 protects the endothelium from ox-LDL-induced endothelial dysfunction partly through competing with miR-22-3p for endogenous RNA. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:3189 / 3196
页数:8
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