College of Life Sciences and Health, Northeastern University, Shenyang, 110169, China; Department of Cardiology and Cardiovascular Research Institute of PLA, General Hospital of Northern Theater Command, Shenyang, 110016, China.
Department of Cardiology and Cardiovascular Research Institute of PLA, General Hospital of Northern Theater Command, Shenyang, 110016, China.
Exp Cell Res. 2023 Jul 1;428(1):113631. doi: 10.1016/j.yexcr.2023.113631. Epub 2023 May 5.
Non-alcoholic fatty liver disease (NAFLD) is one of the main causes of liver disease that has reached its last stage. Over the past few years, evidence for miRNAs' centrality in NAFLD pathogenesis has accumulated. According to some studies, miR-574-5p plays a role in lipid metabolism. However, research on the relationship between miR-574-5p and NAFLD is lacking. For in vivo experiments, we induced the NAFLD mice model with a high-fat diet (HFD). AgomiR-574-5p was injected intravenously into HFD-fed mice for eight weeks, and qPCR was used to identify the expression of miR-574-5p in the serum. In in vitro experiments, The treatment of L-O2 cells with a miR-574-5p mimic resulted in a significant reduction in lipid deposition, suggesting that miR-574-5p can inhibit lipid accumulation and lipid formation induced by OA. The dual-luciferase reporter gene assay revealed that miR-574-5p targets the 3' UTR region of HOXC6 directly. We discovered that OA-induced lipid accumulation in hepatocytes might be mediated through the miR-574-5p-HOXC6 signaling axis. Additional research is required in order to determine the specific mechanism by which HOXC6 downstream pathways are involved in the miR-574-5p induced lipid uptake.
非酒精性脂肪性肝病 (NAFLD) 是一种终末期肝病的主要病因。近年来，miRNA 在 NAFLD 发病机制中的核心作用的证据不断积累。一些研究表明，miR-574-5p 在脂质代谢中发挥作用。然而，关于 miR-574-5p 与 NAFLD 的关系的研究还很缺乏。对于体内实验，我们用高脂肪饮食（HFD）诱导 NAFLD 小鼠模型。用 agomiR-574-5p 静脉注射 HFD 喂养的小鼠 8 周，并用 qPCR 鉴定血清中 miR-574-5p 的表达。在体外实验中，miR-574-5p 模拟物处理 L-O2 细胞导致脂质沉积明显减少，表明 miR-574-5p 可以抑制 OA 诱导的脂质积累和脂质形成。双荧光素酶报告基因检测显示，miR-574-5p 直接靶向 HOXC6 的 3'UTR 区域。我们发现，OA 诱导的肝细胞脂质积累可能是通过 miR-574-5p-HOXC6 信号轴介导的。需要进一步研究以确定 HOXC6 下游途径参与 miR-574-5p 诱导的脂质摄取的具体机制。
