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LINC00460 通过下调 miRNA-24-3p 促进血管内皮细胞的增殖。

LINC00460 Stimulates the Proliferation of Vascular Endothelial Cells by Downregulating miRNA-24-3p.

机构信息

Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Department of Clinical Laboratory Center, Beijing Youan Hospital, Capital Medical University, Beijing, China.

出版信息

Dis Markers. 2022 Feb 18;2022:2524156. doi: 10.1155/2022/2524156. eCollection 2022.

DOI:10.1155/2022/2524156
PMID:35222741
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8881155/
Abstract

OBJECTIVE

To clarify the effect of LINC00460 on mediating the proliferative ability of vascular endothelial cells (ECs) by targeting microRNA-24-3p (miRNA-24-3p), thus influencing the progression of atherosclerotic diseases.

METHODS

Relative levels of LINC00460 and miRNA-24-3p in ECs induced with different doses of ox-LDL (oxidized low density lipoprotein) for different time points were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Influences of LINC00460 and miRNA-24-3p on the viability of ECs were assessed by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assay. Through dual-luciferase reporter gene assay, the binding between LINC00460 and miRNA-24-3p was evaluated. At last, rescue experiments were performed to identify the function of the LINC00460/miRNA-24-3p axis in regulating the proliferative ability of ECs.

RESULTS

LINC00460 was upregulated after ox-LDL treatment in a dose- and time-dependent manner. Viability of ECs gradually increased with the prolongation of ox-LDL treatment and the treatment of increased dose. The overexpression of LINC00460 enhanced the viability and EdU-positive rate in ECs treated with ox-LDL. miRNA-24-3p was the direct target of LINC00460, which was negatively regulated by LINC00460. miRNA-24-3p was downregulated with the prolongation of ox-LDL treatment. The overexpression of miRNA-24-3p could reverse the effect of LINC00460 on regulating the proliferative ability of ECs.

CONCLUSIONS

LINC00460 regulates the proliferative ability of ECs and thus the occurrence and development of coronary atherosclerotic diseases by targeting miRNA-24-3p.

摘要

目的

通过靶向 microRNA-24-3p(miRNA-24-3p),阐明 LINC00460 对血管内皮细胞(ECs)增殖能力的调节作用,从而影响动脉粥样硬化疾病的进展。

方法

采用实时定量聚合酶链反应(qRT-PCR)检测不同浓度 ox-LDL(氧化低密度脂蛋白)作用不同时间点诱导的 ECs 中 LINC00460 和 miRNA-24-3p 的相对水平。通过细胞计数试剂盒-8(CCK-8)和 5-乙炔基-2'-脱氧尿苷(EdU)检测 LINC00460 和 miRNA-24-3p 对 ECs 活力的影响。通过双荧光素酶报告基因实验评估 LINC00460 和 miRNA-24-3p 之间的结合。最后,进行挽救实验以确定 LINC00460/miRNA-24-3p 轴在调节 ECs 增殖能力中的作用。

结果

ox-LDL 处理后,LINC00460 呈剂量和时间依赖性上调。随着 ox-LDL 处理时间的延长和剂量的增加,ECs 的活力逐渐增加。ox-LDL 处理后,LINC00460 的过表达增强了 ECs 的活力和 EdU 阳性率。miRNA-24-3p 是 LINC00460 的直接靶标,受 LINC00460 负调控。ox-LDL 处理时间延长,miRNA-24-3p 下调。miRNA-24-3p 的过表达可以逆转 LINC00460 对调节 ECs 增殖能力的作用。

结论

LINC00460 通过靶向 miRNA-24-3p 调节 ECs 的增殖能力,从而调节冠状动脉粥样硬化性疾病的发生和发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/8fdf92f8166f/DM2022-2524156.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/bc4dc47d40ee/DM2022-2524156.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/9dfb9956d4cc/DM2022-2524156.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/1d4a12da2141/DM2022-2524156.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/8fdf92f8166f/DM2022-2524156.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/bc4dc47d40ee/DM2022-2524156.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/9dfb9956d4cc/DM2022-2524156.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/1d4a12da2141/DM2022-2524156.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0449/8881155/8fdf92f8166f/DM2022-2524156.004.jpg

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