This study aims to investigate the effects of microRNA (miR)‐16/dedicator of cytokinesis 2 (DOCK2) on myocarditis. The differences in the expression of genes in acute myocarditis were filtered out across Gene Expression Omnibus (GEO) database. Myocarditis cell model was established by lipopolysaccharide (LPS) stimulation in cardiomyocytes. The association between miR‐16 and DOCK2 was predicted by bioinformatics software and confirmed by dual‐luciferase assay. Polymerase chain reaction and western blot analysis were employed to assess the expression levels of miR‐16 and DOCK2 under different conditions. Cells viability, apoptosis, and inflammatory reaction were evaluated by Cell Counting Kit‐8, flow cytometry, and enzyme‐linked immunosorbent assays. miR‐16, as an upstream regulator of DOCK2, exhibited lower expression in LPS‐induced myocarditis model. More importantly, we revealed that a marked augmentation of miR‐16 promoted the growth of LPS‐stimulated cardiomyocytes, and attenuated cell apoptosis and inflammatory response. However, an increasing expression of DOCK2 inhibited the remission of LPS‐induced myocardial injury caused by miR‐16 mimic. Herein, our results highlighted that upregulation of miR‐16 resulted in the protective effects on LPS‐induced myocardial injury by reducing DOCK2 expression, affording a pair of novel target molecules for ameliorating the symptoms of myocarditis.

中文翻译：

---

miR-16通过靶向DOCK2抑制细胞凋亡并发挥抗炎作用，在LPS处理的心肌细胞中具有保护功能。

这项研究旨在研究microRNA（miR）-16 /细胞分裂2专用剂（DOCK2）对心肌炎的影响。通过Gene Expression Omnibus（GEO）数据库过滤掉急性心肌炎中基因表达的差异。通过脂多糖（LPS）刺激心肌细胞建立心肌炎细胞模型。miR-16和DOCK2之间的关联已通过生物信息学软件进行了预测，并通过双荧光素酶测定得以证实。聚合酶链反应和蛋白质印迹分析用于评估在不同条件下miR-16和DOCK2的表达水平。通过细胞计数试剂盒-8，流式细胞仪和酶联免疫吸附试验评估了细胞的活力，凋亡和炎症反应。miR-16作为DOCK2的上游调节器，在LPS诱发的心肌炎模型中表现出较低的表达。更重要的是，我们发现miR-16的显着增加促进了LPS刺激的心肌细胞的生长，并减弱了细胞凋亡和炎症反应。但是，DOCK2表达的增加抑制了miR-16模拟物引起的LPS诱导的心肌损伤的缓解。在本文中，我们的结果强调了miR-16的上调通过降低DOCK2的表达对LPS诱导的心肌损伤产生保护作用，从而提供了一对新的靶分子来减轻心肌炎的症状。DOCK2表达的增加抑制了miR-16模拟物引起的LPS诱导的心肌损伤的缓解。在本文中，我们的结果强调了miR-16的上调通过降低DOCK2的表达对LPS诱导的心肌损伤产生保护作用，从而提供了一对新的靶分子来减轻心肌炎的症状。DOCK2表达的增加抑制了miR-16模拟物引起的LPS诱导的心肌损伤的缓解。在本文中，我们的结果强调了miR-16的上调通过降低DOCK2的表达对LPS诱导的心肌损伤产生保护作用，从而提供了一对新的靶分子来减轻心肌炎的症状。