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miR-125b-5p alleviates the damage of myocardial infarction by inhibiting the NFAT2 to reduce F2RL2 expression

    Zhenhua Wu‡

    Academy of Medical Engineering & Translational Medicine, Tianjin University, Tianjin, 300072, China

    ICU, Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    ‡These authors contributed equally to this work

    Search for more papers by this author

    ,
    Jie Geng‡

    CICU, Tianjin Chest Hospital, Tianjin, 300222, China

    ‡These authors contributed equally to this work

    Search for more papers by this author

    ,
    Yunpeng Bai

    Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    ,
    Yujuan Qi

    ICU, Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    ,
    Chao Chang

    ICU, Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    ,
    Yan Jiao

    ICU, Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    &
    Zhigang Guo

    *Author for correspondence:

    E-mail Address: guozhigang_gzg@163.com

    Department of Cardiac Surgery, Tianjin Chest Hospital, Tianjin, 300222, China

    Published Online:https://doi.org/10.2217/rme-2022-0150

    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.

    Plain language summary

    This research proves that miR-125b-5p reduces the level of F2RL2 by preventing the activation of NFAT2 pathway, thereby reducing cardiogenic vascular endothelial cell damage and inflammation (heat, swelling and redness). This may provide a new treatment for heart attacks.

    Graphical abstract

    Papers of special note have been highlighted as: • of interest

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