Myocardial infarction (MI) is a major type of cardiovascular disorder worldwide. In this study, we established a new microRNA (miRNA)-mRNA crosstalk network by integrating data obtained from The National Center for Biotechnology Information Gene Expression Omnibus (NCBI GEO). In addition, functional assays, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and Gene Ontology (GO) analyses, were conducted using the Database for Annotation, Visualization, and Integration Discovery (DAVID). In our study, we generated a new differentially expressed miRNA (DEmiRNA)-differentially expressed gene (DEG) crosstalk network of MI composed of 3 miRNA (miR-489, miR-375, and miR-142-3p) nodes and 163 mRNA nodes. In vitro experiments demonstrated that miR-489 expression was increased in H2O2-treated H9c2 cardiomyocytes in vitro, mimicking myocardial injury. We observed that downregulation of miR-489 reduced H2O2-induced apoptosis, while overexpression of miR-489 had the opposite effects, as revealed by flow cytometry and Western blot analyses. Furthermore, we confirmed the relationship between miR-489 and IGF1 through double luciferase reporter gene assays, which partly explains the antiapoptotic mechanism of miR-489. In conclusion, the experimental results of this study could provide important clues for investigating the mechanism of MI.

中文翻译：

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MiR-489 通过抑制 IGF1 加剧 H2O2 诱导的心肌细胞凋亡。


心肌梗塞（MI）是全世界心血管疾病的一种主要类型。在这项研究中，我们通过整合从国家生物技术信息基因表达综合中心（NCBI GEO）获得的数据建立了一个新的 microRNA (miRNA)-mRNA 串扰网络。此外，还使用注释、可视化和集成发现数据库 (DAVID) 进行功能测定，包括京都基因和基因组百科全书 (KEGG) 途径和基因本体 (GO) 分析。在我们的研究中，我们生成了一个新的 MI 差异表达 miRNA (DEmiRNA)-差异表达基因 (DEG) 串扰网络，由 3 个 miRNA（miR-489、miR-375 和 miR-142-3p）节点和 163 个 mRNA 节点组成。体外实验表明，体外 H2O2 处理的 H9c2 心肌细胞中 miR-489 表达增加，模拟心肌损伤。我们观察到，流式细胞术和蛋白质印迹分析表明，miR-489 的下调减少了 H2O2 诱导的细胞凋亡，而 miR-489 的过表达则具有相反的作用。此外，我们通过双荧光素酶报告基因测定证实了miR-489和IGF1之间的关系，这部分解释了miR-489的抗凋亡机制。总之，本研究的实验结果可以为研究MI的机制提供重要线索。