miR-125b-5p通过抑制NFAT2，降低F2RL2的表达，减轻心肌梗死的损害。

IF 2.4 4区医学 Q4 CELL & TISSUE ENGINEERING

Regenerative medicine Pub Date : 2023-07-01 DOI:10.2217/rme-2022-0150

Zhenhua Wu, Jie Geng, Yunpeng Bai, Yujuan Qi, Chao Chang, Yan Jiao, Zhigang Guo

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引用次数: 0

摘要

目的:探讨miR-125b-5p/活化T细胞核因子1 (NFAT2)/F2RL2对心肌梗死(MI)的影响。方法:通过建立心肌梗死小鼠模型和氧糖剥夺(OGD)诱导的细胞模型，观察NFAT2对心肌梗死过程的影响，测定miR-125b-5p/NFAT2/F2RL2对细胞活力、凋亡及炎症因子水平的影响。结果:NFAT2沉默可减轻心肌梗死模型小鼠的心肌梗死，抑制心肌梗死模型小鼠的炎症反应。在ogd诱导的人冠状动脉内皮细胞和人心脏微血管内皮细胞中，miR-125b-5p增强了细胞活力，但抑制了细胞凋亡、炎症因子和NFAT2水平。NFAT2过表达逆转了miR-125b-5p的作用，而F2RL2沉默抵消了NFAT2过表达的作用。结论:MiR-125b-5p通过抑制NFAT2水平降低F2RL2表达来减轻心肌损伤。

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

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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来源期刊

Regenerative medicine 医学-工程：生物医学

CiteScore

4.20

自引率

3.70%

发文量

审稿时长

6-12 weeks

期刊介绍： Regenerative medicine replaces or regenerates human cells, tissue or organs, to restore or establish normal function*. Since 2006, Regenerative Medicine has been at the forefront of publishing the very best papers and reviews covering the entire regenerative medicine sector. The journal focusses on the entire spectrum of approaches to regenerative medicine, including small molecule drugs, biologics, biomaterials and tissue engineering, and cell and gene therapies – it’s all about regeneration and not a specific platform technology. The journal’s scope encompasses all aspects of the sector ranging from discovery research, through to clinical development, through to commercialization. Regenerative Medicine uniquely supports this important area of biomedical science and healthcare by providing a peer-reviewed journal totally committed to publishing the very best regenerative medicine research, clinical translation and commercialization. Regenerative Medicine provides a specialist forum to address the important challenges and advances in regenerative medicine, delivering this essential information in concise, clear and attractive article formats – vital to a rapidly growing, multidisciplinary and increasingly time-constrained community. Despite substantial developments in our knowledge and understanding of regeneration, the field is still in its infancy. However, progress is accelerating. The next few decades will see the discovery and development of transformative therapies for patients, and in some cases, even cures. Regenerative Medicine will continue to provide a critical overview of these advances as they progress, undergo clinical trials, and eventually become mainstream medicine.