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<p>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&#xa0;min of coronary occlusion followed by 2&#xa0;weeks of reperfusion. The rat AMI model was intravenously administered with control miRNA (9&#xa0;μg/kg), 3&#xa0;μg/kg or 9&#xa0;μg/kg of miR143#12 1&#xa0;h after reperfusion, while the rabbit AMI model was intravenously administered with control miRNA (9&#xa0;μg/kg) or 9&#xa0;μg/kg of miR143#12. In the rat and rabbit AMI models, 9&#xa0;μg/kg of miR143#12 significantly reduced infarct sizes and significantly improved cardiac function including LVEF and LVFS at 2&#xa0;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 H<sub>2</sub>O<sub>2</sub>-induced autophagic cell death by decreasing ROS levels and increased viable cell numbers more than the control by silencing <i>COX-1</i>, -<i>2</i>, and <i>ATG7</i>. 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 <i>COX-1</i> and -<i>2</i>.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月7日

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

摘要

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 H2O2-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.