Department of Cardiovascular Medicine, Chongqing Emergency Medical Center, Chongqing University Central Hospital, Chongqing, 400010, China.
Cell Biochem Biophys. 2024 Jun;82(2):1193-1201. doi: 10.1007/s12013-024-01268-y. Epub 2024 Apr 15.
Multiple RNAs have been involved in the progress of heart failure. However, the role of miR-1268a in heart failure is still unclear. The differentially expressed miRNAs in heart failure was analyzed based on GEO dataset GSE104150. AC16 cells were treated with Angiotensin II (Ang II) to explore the role of miR-1268a in heart failure. The web tool miRWalk was used to analyze the targets of miR-1268a. miR-1268a was up-regulated in Ang II-treated AC16 cells. Ang II treatment markedly inhibited cell proliferation, ATP production, fatty acid (FA) uptake and enhanced levels of HF markers BNP and ST2, and oxidative stress of AC16 cells. Notably, inhibition of miR-1268a eliminated the inhibiting effect of Ang II on cell proliferation, ATP production, FA uptake and decreased levels of BNP an ST2, and oxidative stress on AC16 cells. Furthermore, CD36 was a target of miR-1268a and the CD36 level was decreased by miR-1268a mimics but increased by miR-1268a inhibitor in AC16 cells. miR-1268a regulates FA metabolism and oxidative stress in myocardial cells by targeting CD36 in heart failure.
已有多种 RNA 参与心力衰竭的进展。然而，miR-1268a 在心力衰竭中的作用尚不清楚。基于 GEO 数据集 GSE104150 分析心力衰竭中差异表达的 miRNAs。用血管紧张素 II（Ang II）处理 AC16 细胞，探讨 miR-1268a 在心力衰竭中的作用。使用 miRWalk 网络工具分析 miR-1268a 的靶标。Ang II 处理可上调 AC16 细胞中的 miR-1268a。Ang II 处理可显著抑制 AC16 细胞的增殖、ATP 生成、脂肪酸（FA）摄取，并增强心力衰竭标志物 BNP 和 ST2 的水平，以及细胞的氧化应激。值得注意的是，抑制 miR-1268a 可消除 Ang II 对 AC16 细胞增殖、ATP 生成、FA 摄取的抑制作用，并降低 BNP 和 ST2 的水平，以及细胞的氧化应激。此外，CD36 是 miR-1268a 的靶标，miR-1268a 模拟物可降低 AC16 细胞中的 CD36 水平，而 miR-1268a 抑制剂则可增加其水平。miR-1268a 通过靶向心力衰竭中心肌细胞中的 CD36 来调节 FA 代谢和氧化应激。
