抑制circ_0091761可通过调节miR-1278改善急性心肌梗死诱导的内皮损伤。

IF 2.5 3区 生物学
Bin Zhou, Haitao Wang, Kun Zhang, Jin Xie, Cuicui Yuan, Jia Jin, Jian Zhang, Meng Ma, Zhengnan Zhang
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引用次数: 0

摘要

目的:探讨circ_0091761在急性心肌梗死(AMI)诱导的内皮损伤中的作用。方法:采用缺氧诱导huvec构建AMI细胞模型。可能与circ_0091761相互作用的mirna被ENCORI和circular RNA Interactom数据库识别。采用RT-qPCR方法分析AMI患者中circ_0091761的水平,以及缺氧诱导huvec中miR-1278、ICAM1和VCAM1的水平。流式细胞术检测细胞凋亡。采用ROS试剂盒和LDH试剂盒分别检测ROS和LDH水平。采用双荧光素酶报告基因实验、RIP实验和RNA下拉实验验证circ_0091761和miR-1278之间的相互作用。结果:与健康对照组相比,AMI患者的circ_0091761水平升高。沉默circ_0091761可减少细胞凋亡、ICAM1和VCAM1水平,以及ROS和LDH。circ_0091761可以与miR-1278相互作用,负向调节miR-1278在缺氧诱导的HUVECs中的表达。同时,抑制miR-1278逆转了转染si-circ_0091761对HUVECs的保护作用。结论:下调circ_0091761可通过靶向miR-1278改善ami诱导的内皮细胞损伤。临床试验号:不适用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.

Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.

Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.

Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.

Objective: The main objective of the article was to explore the role of circ_0091761 in acute myocardial infarction (AMI)-induced endothelial injury.

Methods: A cellular model of AMI was constructed by hypoxia-induced HUVECs. miRNAs that may interact with circ_0091761 were recognized by the ENCORI and circular RNA Interactom databases. RT-qPCR was performed to analyze the levels of circ_0091761 in AMI patients as well as miR-1278, ICAM1, and VCAM1 in hypoxia-induced HUVECs. Flow cytometry was used to detect apoptosis. ROS kit and LDH kit were used to detect the levels of ROS and LDH, respectively. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were performed to validate their interaction between circ_0091761 and miR-1278.

Results: circ_0091761 was elevated in AMI patients compared to healthy controls. Silencing circ_0091761 reduced apoptosis, ICAM1, and VCAM1 levels, as well as ROS and LDH. circ_0091761 could interact with miR-1278 and negatively regulate miR-1278 expression in hypoxia-induced HUVECs. At the same time, inhibiting miR-1278 reverses the protective effect of transfected si-circ_0091761 on HUVECs.

Conclusion: Down-regulation of circ_0091761 ameliorates AMI-induced endothelial injury by targeting miR-1278.

Clinical trial number: Not applicable.

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来源期刊
Hereditas
Hereditas Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍: For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.
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