MiR-125b-5p Alleviates the Damage of Myocardial Infarction by Inhibiting the NFAT2 to Reduce F2RL2 Expression

作者：Zhenhua Wu, Jie Geng, Yunpeng Bai, Yujuan Qi, Chao Chang, Yan Jiao, Zhigang Guo · 发表于：Regenerative Medicine · 年份：2023 · DOI：10.2217/rme-2022-0150 · 被引用次数：11 · 研究领域：Signaling Pathways in Disease、Circular RNAs in diseases、MicroRNA in disease regulation

Aim: To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 (NFAT2)/F2RL2 on myocardial infarction (MI). Method: After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of NFAT2 on the process of MI were observed, the effects of miR-125b-5p/NFAT2/F2RL2 on the cell viability, apoptosis, and inflammatory factors levels were determined. Result: NFAT2 silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while F2RL2 silencing offset the effects of NFAT2 overexpression. Conclusion: MiR-125b-5p alleviates MI injury by inhibiting NFAT2 level to reduce F2RL2 expression.