Jiang Hongfei, Gong Ren, Wu Yanqing
Department of Cardiology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Exp Ther Med. 2022 Mar;23(3):243. doi: 10.3892/etm.2022.11168. Epub 2022 Jan 27.
The mechanisms underlying gene therapy for the treatment of cardiovascular diseases remain to be elucidated. microRNAs (miRs) have been recognized as key regulators in vascular smooth muscle cells, which are involved in the formation of atherosclerosis. The present study aimed to explore the role of miR-129-5p in the regulation of high-mobility group box 1 protein (HMGB1) and the PI3k/Akt signaling pathway, and further explore the role of miR-129-5p in the viability and migration of A7r5 cells induced by oxidized low-density lipoprotein (ox-LDL). Cell viability, viability and migration were determined using Cell Counting Kit-8, colony formation, wound healing and Transwell assays. The expression levels of miR-129-5p and HMGB1 were detected using reverse transcription-quantitative PCR and western blotting. A dual-luciferase assay was used to confirm the association between miR-129-5p and HMGB1. RT-qPCR results in the present study demonstrated that the expression levels of miR-129-5p in A7r5 cells induced by ox-LDL were significantly decreased, compared with the control cells. Moreover, the viability and migration of A7r5 cells induced by ox-LDL were increased compared with control group. Western blot and RT-qPCR results showed that miR-129-5p decreased the expression of HMGB1 in A7r5 cells compared with control group. The present results demonstrated that miR-129-5p inhibited the viability, viability and migration of A7r5 cells induced by ox-LDL, and directly targeted HMGB1 to regulate the PI3k/Akt signaling pathway. In conclusion, miR-129-5p inhibited the PI3k/Akt signaling pathway by directly targeting HMGB1, and reduced the viability, viability and migration of A7r5 cells induced by ox-LDL.
用于治疗心血管疾病的基因治疗的潜在机制仍有待阐明。微小RNA（miR）已被公认为血管平滑肌细胞中的关键调节因子，参与动脉粥样硬化的形成。本研究旨在探讨miR-129-5p在调节高迁移率族蛋白B1（HMGB1）和PI3k/Akt信号通路中的作用，并进一步探讨miR-129-5p在氧化型低密度脂蛋白（ox-LDL）诱导的A7r5细胞活力和迁移中的作用。使用细胞计数试剂盒-8、集落形成、伤口愈合和Transwell实验来测定细胞活力、活力和迁移。使用逆转录定量PCR和蛋白质印迹法检测miR-129-5p和HMGB1的表达水平。采用双荧光素酶报告基因实验来证实miR-129-5p与HMGB1之间的关联。本研究中的逆转录定量PCR结果表明，与对照细胞相比，ox-LDL诱导的A7r5细胞中miR-129-5p的表达水平显著降低。此外，与对照组相比，ox-LDL诱导的A7r5细胞的活力和迁移增加。蛋白质印迹和逆转录定量PCR结果显示，与对照组相比，miR-129-5p降低了A7r5细胞中HMGB1的表达。本研究结果表明，miR-129-5p抑制了ox-LDL诱导的A7r5细胞的活力、活力和迁移，并直接靶向HMGB1以调节PI3k/Akt信号通路。总之，miR-129-5p通过直接靶向HMGB1抑制PI3k/Akt信号通路，并降低了ox-LDL诱导的A7r5细胞的活力、活力和迁移。
