Research Paper Volume 13, Issue 18 pp 22276—22285

Improvement of cardiac function by mesenchymal stem cells derived extracellular vesicles through targeting miR-497/Smad7 axis

Min Chen2, *, , Jianfei Chen2, *, , Caiting Li1, , Ranjie Yu1, , Weiwen Chen3, , Cunrong Chen1, *, ,

  • 1 Department of Critical Care Medicine, Union Hospital of Fujian Medical University, Fuzhou 350001, Fujian, China
  • 2 Department of Critical Care Medicine, Affiliated Hospital of Putian University, Putian 351100, Fujian, China
  • 3 Department of Intensive Care Unit, Quan Zhou First Hospital Affiliated to Fujian Medical University, Quanzhou 362000, Fujian, China
* Equal contribution

Received: May 12, 2021       Accepted: August 17, 2021       Published: September 16, 2021
How to Cite

Copyright: © 2021 Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Background: The extracellular vesicles (EVs) secreted by bone marrow mesenchymal stromal cells (MSCs) have the ability to improve Myocardial infarction (MI). Some microRNAs (miRNAs) including miR-497 and related target genes have been proved to be closely linked with heart diseases. However, EVs could regulate MI process through miR-497, and the mechanisms have not been fully reported.

Methods: Ligation of left anterior descending artery was performed to established MI animals model. Hypoxia cell model was established through lowering the level of oxygen. The cell invasion, migration, and proliferation were measured using tanswell, wound heating, and MTT assays. HE, Masson trichrome, and Sirius Red staining were used to investigate the morphological changes.

Results: Overexpression of miR-497 reversed the promotion of cell migration, invasion, and proliferation caused by EVs. The improvement of cardiac function induced by EVs could also be reversed by overexpression of miR-497. Direct binding site between Smad7 and miR-497 was identified. Knockdown of Smad7 reversed the improvement of cardiac function induced by EVs.

Conclusions: We found that EVs isolated from MSCs might improve the cardiac injury caused by MI through targeting miR497/Smad7. This study provides novel potential therapeutic thought for the prevention and treatment of MI through targeting miR-497/Smad7.


MI: Myocardial infarction; SD: Standard deviation; RT-PCR: Real-time polymerase chain reaction; HE: Hematoxylin-eosin; EVs: Extracellular vesicles; MSCs: Mesenchymal stromal cells; miRNA: microRNAs.