文章摘要:circABCA3敲低通过靶向miR-671-5p/PCSK9轴缓解缺氧诱导的人心脏微血管内皮细胞功能障碍。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2023-11-01 Epub Date: 2023-09-07 DOI:10.1007/s12192-023-01377-2
Hui Hui, Gaowa Zhao, Mingliang Du, Qin Yu
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摘要

内皮细胞功能障碍是急性心肌梗死(AMI)发展的重要阶段之一。然而,circABCA3 (hsa_circ_0037516)是否通过调节内皮细胞功能障碍介导AMI的发展尚不清楚。使用GEO数据库(GSE169594和GSE160717)筛选差异表达的环状rna。采用缺氧诱导的人心脏微血管内皮细胞(HCMECs)模拟AMI细胞模型。采用实时荧光定量PCR检测circABCA3、microRNA (miR)-671-5p、蛋白转化酶subtilisin/ keexin type 9 (PCSK9)的表达。采用细胞计数试剂盒8法、EdU法、transwell法、伤口愈合法、成管法和流式细胞术检测细胞增殖、迁移、血管生成和凋亡。采用双荧光素酶报告基因试验和RIP试验验证RNA相互作用。western blot检测PCSK9蛋白及凋亡相关标志物的表达情况。根据GEO数据库筛选,circABCA3是AMI患者血液样本中高表达的circRNA。circABCA3在AMI患者和缺氧诱导的HCMECs中过表达。在缺氧诱导的HCMECs中,circABCA3的沉默增强了增殖、迁移和血管生成,并抑制了细胞凋亡。circABCA3海绵miR-671-5p正向调节PCSK9的表达。miR-671-5p抑制剂或PCSK9过表达推翻了circABCA3敲低对缺氧诱导的HCMEC功能障碍的调节。circABCA3可能是缓解AMI过程的潜在靶点,其中敲低通过调节miR-671-5p/PCSK9轴缓解缺氧诱导的HCMEC功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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RETRACTED ARTICLE: circABCA3 knockdown relieves hypoxia-induced human cardiac microvascular endothelial cell dysfunction by targeting the miR-671-5p/PCSK9 axis.
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