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化学修饰的微小RNA-143-3p对动物模型急性心肌梗死的修复作用

Restoration effect of chemically modified microRNA-143-3p on acute myocardial infarction in animal models.

作者信息

Minatoguchi Shingo, Sugito Nobuhiko, Heishima Kazuki, Ito Yuko, Nakashima Remi, Okura Hiroyuki, Akao Yukihiro, Minatoguchi Shinya

机构信息

Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan.

United Graduate School of Drug Discovery and Medical Information Sciences, Gifu University, Gifu, Japan.

出版信息

Sci Rep. 2025 Jan 7;15(1):1107. doi: 10.1038/s41598-024-76429-3.

DOI:10.1038/s41598-024-76429-3
PMID:39774185
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11707079/
Abstract

We investigated whether miR143#12, a synthesized chemically modified miR-143-3p derivative, exerts therapeutic effects on acute myocardial infarction (AMI). Sprague-Dawley rats and Japanese white rabbits underwent 30 min of coronary occlusion followed by 2 weeks of reperfusion. The rat AMI model was intravenously administered with control miRNA (9 μg/kg), 3 μg/kg or 9 μg/kg of miR143#12 1 h after reperfusion, while the rabbit AMI model was intravenously administered with control miRNA (9 μg/kg) or 9 μg/kg of miR143#12. In the rat and rabbit AMI models, 9 μg/kg of miR143#12 significantly reduced infarct sizes and significantly improved cardiac function including LVEF and LVFS at 2 weeks. The tissue miR143 levels in infarct areas significantly decreased after AMI in both models. Electron microscopic study and immunohistochemistry suggested that miR143#12 suppressed autophagic cell death caused by AMI and induced neoangiogenesis in the infarct border. In cultured rat H9c2 cells, miR143#12 significantly inhibited HO-induced autophagic cell death by decreasing ROS levels and increased viable cell numbers more than the control by silencing COX-1, -2, and ATG7. Replacement treatment with miR143#12 in the infarct areas, where the expression levels of miR143 were significantly decreased, has a beneficial effect on AMI by silencing COX-1 and -2.

摘要

我们研究了化学合成修饰的miR - 143 - 3p衍生物miR143#12对急性心肌梗死（AMI）是否具有治疗作用。将Sprague - Dawley大鼠和日本白兔进行30分钟的冠状动脉闭塞，随后再灌注2周。在大鼠AMI模型中，再灌注1小时后静脉注射对照miRNA（9μg/kg）、3μg/kg或9μg/kg的miR143#12，而在兔AMI模型中，静脉注射对照miRNA（9μg/kg）或9μg/kg的miR143#12。在大鼠和兔AMI模型中，9μg/kg的miR143#12在2周时显著减小梗死面积，并显著改善心脏功能，包括左心室射血分数（LVEF）和左心室短轴缩短率（LVFS）。在两个模型中，AMI后梗死区域的组织miR143水平均显著降低。电子显微镜研究和免疫组织化学表明，miR143#12抑制AMI引起的自噬性细胞死亡，并在梗死边缘诱导新生血管形成。在培养的大鼠H9c2细胞中，miR143#12通过降低活性氧水平显著抑制血红素加氧酶（HO）诱导的自噬性细胞死亡，并且通过沉默环氧化酶 - 1（COX - 1）、 - 2和自噬相关蛋白7（ATG7），使存活细胞数量比对照组增加更多。在miR143表达水平显著降低的梗死区域用miR143#12进行替代治疗，通过沉默COX - 1和 - 2对AMI具有有益作用。

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