基因沉默
细胞凋亡
炎症
活力测定
心肌梗塞
细胞
癌症研究
细胞生物学
化学
医学
内科学
生物
生物化学
基因
作者
Zhenhua Wu,Jie Geng,Yunpeng Bai,Yujuan Qi,Chao Chang,Yan Jiao,Zhigang Guo
出处
期刊:Regenerative Medicine
[Future Medicine]
日期:2023-06-21
卷期号:18 (7): 543-559
被引量:4
标识
DOI:10.2217/rme-2022-0150
摘要
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.
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