An increasing amount of research showed that endothelial cells (ECs) play crucial role in vascular disorders such as atherosclerosis (AS). LncRNA OIP5-AS1 and microRNA-320a (miR-320a) were reported to exert function in ECs. The purpose of this research was to investigate the functional mechanism of OIP5-AS1 and miR-320a in ox-LDL-treated HUVECs. The RNA levels of OIP5-AS1, miR-320a, and Lectin-like oxidized low-density lipoprotein receptor 1 (LOX1) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The protein levels of LOX1 and cell apoptosis-related genes were determined by Western blot assay. In addition, Cell Counting Kit-8 (CCK-8) and flow cytometry analysis were used to assess cell viability and apoptosis, respectively. Lactate dehydrogenase (LDH) activity was measured using LDH release assay. Besides, the interaction between miR-320a and OIP5-AS1 or LOX1 was predicted by starbase and verified by the dual-luciferase reporter assay. OIP5-AS1 expression was increased and miR-320a expression was decreased in oxidative low-density lipoprotein (ox-LDL)-treated HUVECs. OIP5-AS1 knockdown upregulated ox-LDL-treated HUVECs viability and suppressed apoptosis as well as LDH release. Interestingly, OIP5-AS1 elevated LOX1 level through downregulating miR-320a expression. As expected, miR-320a modulated LOX1 expression to mediate ox-LDL-treated HUVECs progression. Furthermore, OIP5-AS1 knockdown modulated cell progression via regulating miR-320a/LOX1 axis in ox-LDL-treated HUVECs. Our results demonstrated that the depletion of OIP5-AS1 enhanced cell viability and repressed apoptosis as well as LDH release in ox-LDL-treated HUVECs, providing potential target for the treatment of AS.

中文翻译：

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LNCRNA OIP5-AS1通过miR-320a / LOX1轴调节氧化型低密度脂蛋白介导的内皮细胞损伤。

越来越多的研究表明，内皮细胞（EC）在诸如动脉粥样硬化（AS）的血管疾病中起关键作用。据报道，LncRNA OIP5-AS1和microRNA-320a（miR-320a）在EC中发挥功能。这项研究的目的是研究OIP5-AS1和miR-320a在ox-LDL处理的HUVEC中的功能机制。通过实时定量聚合酶链反应（qRT-PCR）检测OIP5-AS1，miR-320a和凝集素样的氧化型低密度脂蛋白受体1（LOX1）的RNA水平。通过蛋白质印迹法测定LOX1的蛋白水平和细胞凋亡相关基因。此外，Cell Counting Kit-8（CCK-8）和流式细胞仪分析分别用于评估细胞活力和凋亡。乳酸脱氢酶（LDH）活性使用LDH释放测定法进行测量。除了，starR预测了miR-320a与OIP5-AS1或LOX1之间的相互作用，并通过双荧光素酶报告基因检测法进行了验证。在氧化低密度脂蛋白（ox-LDL）处理的HUVEC中，OIP5-AS1表达增加，而miR-320a表达减少。OIP5-AS1敲低上调了ox-LDL处理的HUVEC的活力，并抑制了细胞凋亡以及LDH的释放。有趣的是，OIP5-AS1通过下调miR-320a表达来提高LOX1水平。如预期的那样，miR-320a调节LOX1表达以介导ox-LDL处理的HUVEC的进展。此外，OIP5-AS1敲低通过调节ox-LDL处理的HUVEC中的miR-320a / LOX1轴来调节细胞进程。我们的研究结果表明，OIP5-AS1的耗竭可增强细胞活力，并抑制经ox-LDL处理的HUVEC中的细胞凋亡以及LDH的释放，