Department of Medical Genetics, College of Basic Medical Science, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, China.
Department of Clinical Genetics, Shengjing Hospital of China Medical University, No. 36 San Hao Street, Shenyang, China.
J Immunol Res. 2018 Aug 26;2018:6140320. doi: 10.1155/2018/6140320. eCollection 2018.
Thioredoxin reductase (TrxR), an antioxidant enzyme dependent on nicotinamide adenine dinucleotide phosphate, plays a vital role in defense against oxidative stress. However, the role of microRNAs targeting TrxR under oxidative stress has not yet been determined. In this study, we tested the involvement of miRNA-mediated posttranscriptional regulation in HO-induced TrxR1 expression in endothelial cells. Dual luciferase assay combined with expression analysis confirmed that miR-125a suppressed TrxR1 expression by targeting its 3'-UTR. Furthermore, HO induced TrxR1 expression partly through downregulation of miR-125a. These findings indicate that miRNA-mediated posttranscriptional mechanism is involved in HO-induced TrxR1 expression in endothelial cells, suggesting an important role of miRNAs in the response to oxidative stress.
硫氧还蛋白还原酶（TrxR）是一种依赖烟酰胺腺嘌呤二核苷酸磷酸的抗氧化酶，在抵抗氧化应激中起着至关重要的作用。然而，在氧化应激下靶向 TrxR 的 microRNAs 的作用尚不清楚。在这项研究中，我们测试了 microRNA 介导的转录后调控在 HO 诱导的内皮细胞 TrxR1 表达中的作用。双荧光素酶报告基因实验结合表达分析证实 miR-125a 通过靶向 TrxR1 的 3'UTR 抑制其表达。此外，HO 通过下调 miR-125a 诱导 TrxR1 表达。这些发现表明，miRNA 介导的转录后机制参与了 HO 诱导的内皮细胞 TrxR1 表达，提示 miRNA 在应对氧化应激中的重要作用。
