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Background <p>Transplantation of endothelial progenitor cells (EPCs) has been reported to ameliorate myocardial injury after acute myocardial infarction (AMI). Evidence suggests that microRNA (miR)-16-5p can aggravate AMI progression. This study aims to examine whether it affects the efficacy of EPCs in AMI.</p> Methods <p>Mouse bone marrow-derived EPCs were identified by DiL-ac-LAL uptake assay and flow cytometry. Lentiviruses carrying miR-16-5p inhibitor or the scrambled control were transduced into EPCs. Luciferase reporter assay was implemented to elucidate the interaction between miR-16-5p and its target Plxna4. RT-qPCR and western blotting were utilized for the detection of RNA or protein levels, respectively. Wound healing and tube formation assays were implemented to assess EPC migration and angiogenesis. A mouse AMI model was established by ligating the left anterior descending coronary artery. Murine heart tissues were harvested for Masson’s trichrome staining and immunostaining.</p> Results <p>miR-16-5p targeted Plxna4 in EPCs. miR-16-5p depletion facilitated EPC migration, tube formation, and VEGF expression, whereas these effects were reversed by Plxna4 silencing. Moreover, miR-16-5p inhibition augmented the therapeutic efficacy of EPCs in ameliorating AMI in mice. miR-16-5p expression and Plxna4 expression were negatively correlated in AMI murine hearts.</p> Conclusion <p>miR-16-5p inhibition facilitates EPC migration and angiogenesis and enhances the efficacy of EPCs in improving cardiac function and promoting neovascularization after AMI.</p>

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Transplantation of miR-16-5p Inhibitor-Modified Endothelial Progenitor Cells Improves Acute Myocardial Infarction by Promoting Vascular Regeneration

  • 期刊论文

  • 发表日期：

    2025年11月18日

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  • Qinqin Wu,
  • Benling Qi,
  • Fengqin Yan,
  • Yingxia He,
  • Shan Sun,
  • Hanqing Liu,
  • Hong Zhu

摘要

Background

Transplantation of endothelial progenitor cells (EPCs) has been reported to ameliorate myocardial injury after acute myocardial infarction (AMI). Evidence suggests that microRNA (miR)-16-5p can aggravate AMI progression. This study aims to examine whether it affects the efficacy of EPCs in AMI.

Methods

Mouse bone marrow-derived EPCs were identified by DiL-ac-LAL uptake assay and flow cytometry. Lentiviruses carrying miR-16-5p inhibitor or the scrambled control were transduced into EPCs. Luciferase reporter assay was implemented to elucidate the interaction between miR-16-5p and its target Plxna4. RT-qPCR and western blotting were utilized for the detection of RNA or protein levels, respectively. Wound healing and tube formation assays were implemented to assess EPC migration and angiogenesis. A mouse AMI model was established by ligating the left anterior descending coronary artery. Murine heart tissues were harvested for Masson’s trichrome staining and immunostaining.

Results

miR-16-5p targeted Plxna4 in EPCs. miR-16-5p depletion facilitated EPC migration, tube formation, and VEGF expression, whereas these effects were reversed by Plxna4 silencing. Moreover, miR-16-5p inhibition augmented the therapeutic efficacy of EPCs in ameliorating AMI in mice. miR-16-5p expression and Plxna4 expression were negatively correlated in AMI murine hearts.

Conclusion

miR-16-5p inhibition facilitates EPC migration and angiogenesis and enhances the efficacy of EPCs in improving cardiac function and promoting neovascularization after AMI.