The heart is one of the most common organs involved in sepsis-induced organ dysfunction and about 50% septic patients complicated with myocardial injury. So far, the molecular mechanisms underlying sepsis-induced cardiac damage remain unclear. In this study we aimed to evaluate the effect of miR-642a on sepsis-induced cardiac injury in vitro and explore the possible lncRNA-microRNA mechanism. We first downloaded GSE101639 to identify differentially expressed genes (DEGs) in sepsis. The expression of miR-642a in LPS-induced H9C2 cells was detected by qRT-PCR. MTT assay, cell migration, flow cytometry analysis, ELISA, qRT-PCR and Western blotting analysis were applied to evaluating the effect of miR-642a mimic on LPS-induced H9C2 cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. The results showed miR-642a expression was decreased in septic patients and LPS-induced H9C2 cells. Besides, MiR-642a mimic promoted cell viability and migration, inhibited cell apoptosis of LPS-induced H9C2 cells. Bioinformatics analysis showed miR-642a directly targets with 3’-UTR of ROCK1. Moreover, LUCAT1 regulated ROCK1 expression act as a competing endogenous RNA (ceRNA) for miR-642a. Our data demonstrated that lncRNA LUCAT1 could function via sponging miR-642a to regulate ROCK1 expression in LPS-induced H9C2 cells. And knockdown of lncRNA LUCAT1 could suppress LPS-induced cardiac injury in vitro.

心脏是脓毒症引起的器官功能障碍最常见的器官之一，约50%的脓毒症患者并发心肌损伤。到目前为止，脓毒症引起的心脏损伤的分子机制仍不清楚。在本研究中，我们旨在评估 miR-642a 在体外对脓毒症诱导的心脏损伤的影响，并探索可能的 lncRNA-microRNA 机制。我们首先下载了 GSE101639 来识别脓毒症中的差异表达基因 (DEG)。通过qRT-PCR检测LPS诱导的H9C2细胞中miR-642a的表达。应用MTT法、细胞迁移、流式细胞术分析、ELISA、qRT-PCR和Western印迹分析来评估miR-642a模拟物对LPS诱导的H9C2细胞的影响。生物信息学分析和救援实验致力于其潜在机制。结果显示，脓毒症患者和 LPS 诱导的 H9C2 细胞中 miR-642a 的表达降低。此外，MiR-642a 模拟物促进细胞活力和迁移，抑制 LPS 诱导的 H9C2 细胞的细胞凋亡。生物信息学分析显示 miR-642a 直接靶向 ROCK1 的 3'-UTR。此外，LUCAT1 调节 ROCK1 表达作为 miR-642a 的竞争性内源性 RNA (ceRNA)。我们的数据表明，lncRNA LUCAT1 可以通过海绵化 miR-642a 来调节 LPS 诱导的 H9C2 细胞中 ROCK1 的表达。并且lncRNA LUCAT1的敲低可以在体外抑制LPS诱导的心脏损伤。生物信息学分析显示 miR-642a 直接靶向 ROCK1 的 3'-UTR。此外，LUCAT1 调节 ROCK1 表达作为 miR-642a 的竞争性内源性 RNA (ceRNA)。我们的数据表明，lncRNA LUCAT1 可以通过海绵化 miR-642a 来调节 LPS 诱导的 H9C2 细胞中 ROCK1 的表达。并且lncRNA LUCAT1的敲低可以在体外抑制LPS诱导的心脏损伤。生物信息学分析显示 miR-642a 直接靶向 ROCK1 的 3'-UTR。此外，LUCAT1 调节 ROCK1 表达作为 miR-642a 的竞争性内源性 RNA (ceRNA)。我们的数据表明，lncRNA LUCAT1 可以通过海绵化 miR-642a 来调节 LPS 诱导的 H9C2 细胞中 ROCK1 的表达。并且lncRNA LUCAT1的敲低可以在体外抑制LPS诱导的心脏损伤。