Department of Cardiovascular Surgery, Henan Provincial People's Hospital, Zhengzhou 450003, PR China.
ICU of Cardiovascular Surgery, Henan Provincial People's Hospital, Zhengzhou 450003, PR China.
Int J Cardiol. 2019 Apr 1;280:152-159. doi: 10.1016/j.ijcard.2018.12.077. Epub 2019 Jan 4.
Myocardial infarction (MI) is a common cardiovascular disease caused by myocardial ischemia. Also, microRNA (miRNA) participates in the pathophysiology of many cardiovascular diseases, which can affect stem cell transplantation in the treatment of MI. In this study, our aim is to explore effect of miR-26b on inflammatory response and myocardial remodeling through the MAPK pathway by targeting PTGS2 in mice with MI.
Microarray data analysis was conducted to screen MI-related differentially expressed gens (DEGs). Relationship between miR-26b and PTGS2 was testified. Cardiac function, inflammatory reaction, infarct size, and myocardial fibrosis were observed. The miR-26b expression and mRNA and protein levels of, PTGS2, ERK, JNK and p38 and Bcl-2/Bax were examined. The effect of miR-26b on cell apoptosis was also analyzed.
MiR-26b was predicted to target PTGS2 further to mediate the MAPK pathway, thus affecting MI. MiR-26b negatively targeted PTGS2. MI mice showed decreased cardiac function, as well as increased inflammatory reaction, myocardial injury, area of fibrosis and myocardial cell apoptosis. After injection of miR-26b agomir or NS-398 (PTGS2 inhibitor), inflammatory response of MI mice was attenuated and myocardial remodeling induced by MI was alleviated.
These findings indicate that miR-26b inhibits PTGS2 to activate the MAPK pathway, so as to reduce inflammatory response and improve myocardial remodeling in mice with MI.
心肌梗死（MI）是一种由心肌缺血引起的常见心血管疾病。此外，microRNA（miRNA）参与许多心血管疾病的病理生理过程，可能会影响 MI 治疗中的干细胞移植。在这项研究中，我们的目的是通过靶向 PTGS2 来探讨 miR-26b 通过 MAPK 通路对 MI 小鼠炎症反应和心肌重构的影响。
进行微阵列数据分析以筛选与 MI 相关的差异表达基因（DEGs）。验证 miR-26b 与 PTGS2 之间的关系。观察心功能、炎症反应、梗死面积和心肌纤维化。检测 miR-26b 的表达以及 PTGS2、ERK、JNK 和 p38 的 mRNA 和蛋白水平和 Bcl-2/Bax。还分析了 miR-26b 对细胞凋亡的影响。
miR-26b 被预测可靶向 PTGS2 进一步介导 MAPK 通路，从而影响 MI。miR-26b 负向靶向 PTGS2。MI 小鼠表现出心功能下降，以及炎症反应增强、心肌损伤、纤维化面积增加和心肌细胞凋亡增加。注射 miR-26b agomir 或 NS-398（PTGS2 抑制剂）后，MI 小鼠的炎症反应减轻，MI 引起的心肌重构得到缓解。
这些发现表明，miR-26b 通过抑制 PTGS2 激活 MAPK 通路，从而减少 MI 小鼠的炎症反应并改善心肌重构。
