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Hypoxia-challenged MSC-derived exosomes deliver miR-210 to attenuate post-infarction cardiac apoptosis
Hao Cheng1, Shufu Chang1, Rende Xu1
1Department of Cardiology, Zhongshan Hospital, Fudan University, 1609 Xietu Road, Shanghai, 200032, China.
Insights
Mesenchymal stem cell (MSC) exosomes carrying miR-210 protect heart cells from damage after myocardial infarction (MI). This therapy reduces infarct size and improves heart function by transferring miR-210 to protect cardiomyocytes.
Area of Science:
- Cardiovascular Biology
- Stem Cell Biology
- Exosome Biology
Background:
- Myocardial infarction (MI) remains a leading cause of mortality globally.
- Existing treatments for MI, while life-prolonging, do not fully restore cardiac function due to limited cardiomyocyte regenerative capacity.
- Mesenchymal stem cells (MSCs) show therapeutic potential for MI, but the mechanisms underlying their beneficial effects are under investigation.
Purpose of the Study:
- To investigate the role of mesenchymal stem cell (MSC)-derived exosomes in protecting cardiomyocytes from apoptosis.
- To determine if exosomal microRNA-210 (miR-210) mediates the cardioprotective effects of MSCs after myocardial infarction (MI).
- To evaluate the therapeutic potential of MSC-derived exosomes enriched with miR-210 in an in vivo model of MI.
Main Methods:
- MSCs were isolated, and exosomes were purified and characterized.
- Microarray analysis was performed to identify exosomal microRNAs, focusing on miR-210.
- Gain- and loss-of-function studies were conducted in vitro and in vivo to assess the impact of exosomes and exosomal miR-210 on cardiomyocyte survival, proliferation, and cardiac function post-MI.
Main Results:
- MSC-derived exosomes significantly reduced infarct size and improved cardiac function in a mouse model of MI.
- In vitro experiments demonstrated that MSC exosomes enhanced cardiomyocyte survival under hypoxic conditions.
- Dual-luciferase reporter assays identified AIFM3 as a downstream target of miR-210, and miR-210 overexpression in exosomes augmented cardioprotection.
Conclusions:
- Mesenchymal stem cell (MSC)-derived exosomes exert significant cardioprotective effects following myocardial infarction (MI).
- The therapeutic benefits are, at least in part, mediated by the transfer of exosomal miR-210 to cardiomyocytes.
- Exosomal miR-210 represents a promising therapeutic agent for mitigating cardiac damage after MI.
Background:
Myocardial infarction (MI) is a major cause of death worldwide. Although percutaneous coronary intervention and coronary artery bypass grafting can prolong life, cardiac damage persists. In particular, cardiomyocytes have no regenerative capacity. Mesenchymal stem cells (MSCs) are attractive candidates for the treatment of MI. The manner by which MSCs exert a beneficial effect upon injured cells is a source of continued study.
Methods:
After the isolation and identification of exosomes from MSCs, the expression of miR-210 was determined by microarray chip. Subsequently, gain- and loss-function approaches were conducted to detect the role of exosomes and exosomal-miR-210 in cell proliferation and apoptosis of cardiomyocytes, as well as the MI in vivo. Dual-Luciferase Report Gene System was used to demonstrate the target gene of miR-210.
Results:
We tested the hypothesis that MSC-derived exosomes transfer specific miRNA to protect cardiomyocytes from apoptotic cell death. Interestingly, direct cardiac injection of MSC exosomes reduced infarct size and improved heart function after coronary ligation. In vitro, the MSC exosomes enhanced cardiomyocyte survival to hypoxia. Confirmation of exosome uptake in myocytes was confirmed. Dual-luciferase reporter assay implicated miR-210 as a mediator of the therapeutic effect and AIFM3 as a downstream target. Treatment with miR-210 overexpressing MSC exosomes improved myocyte protection to both in vitro and in vivo stress. Furthermore, the endogenous and exogenous miR-210 had the same therapeutic effects.
Conclusion:
These results demonstrated that the beneficial effects offered by MSC-exosomes transplantation after MI are at least partially because of excreted exosome containing mainly miR-210.
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