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Purification and Transplantation of Myogenic Progenitor Cell Derived Exosomes to Improve Cardiac Function in Duchenne Muscular Dystrophic Mice
Published on: April 10, 2019
Extracellular vesicles derived from microRNA-150-5p-overexpressing mesenchymal stem cells protect rat hearts against
Hesheng Ou1, Hongli Teng1, Yuwang Qin1
1Section of Science and Technology, Guangxi International Zhuang Medicine Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning 530201, P.R. China.
Abstract:
An intriguing area of research has demonstrated the ability of extracellular vesicles (EVs) as biological vehicles for microRNAs (miRNAs) transfer. Mesenchymal stem cells (MSCs) produce large amounts of EVs. Rat models of ischemia/reperfusion (I/R) were established to explore the expression profile of thioredoxin-interacting protein (TXNIP), which was then knocked-down to investigate its effects on myocardial remodeling, followed by detection on myocardial infarction size (MIS), myocardial collagen volume fraction (CVF) and cardiomyocyte apoptosis. MSCs-derived EVs carrying miR-150-5p were cultured with neonatal cardiomyocytes under hypoxia/hypoglycemia condition for in vitro exploration and intramyocardially injected into I/R rats for in vivo exploration. I/R-induced rats presented higher TXNIP levels and lower miR-150-5p levels, along with increased cardiomyocyte apoptosis. miR-150-5p in MSCs was transferred through EVs to cardiomyocytes, leading to suppressed myocardial remodeling, as reflected by smaller MIS and CVF and suppressed cardiomyocyte apoptosis. I/R-treated rats injected with MSCs-derived EVs containing miR-150-5p showed a reduction in myocardial remodeling associated with the downregulation of TXNIP, which may be clinically applicable for treatment of I/R.
Insights
Mesenchymal stem cell-derived extracellular vesicles carrying miR-150-5p can reduce myocardial remodeling after ischemia/reperfusion injury. This transfer suppresses thioredoxin-interacting protein, offering a potential therapeutic strategy for heart attack treatment.
Area of Science:
- Cardiovascular Research
- Stem Cell Biology
- Extracellular Vesicle Biology
Background:
- Extracellular vesicles (EVs) mediate microRNA (miRNA) transfer between cells.
- Mesenchymal stem cells (MSCs) are a rich source of EVs.
- Ischemia/reperfusion (I/R) injury leads to myocardial remodeling and cardiomyocyte apoptosis.
Purpose of the Study:
- To investigate the role of thioredoxin-interacting protein (TXNIP) in I/R-induced myocardial remodeling.
- To explore the therapeutic potential of MSCs-derived EVs carrying miR-150-5p in I/R injury.
- To elucidate the mechanism of miR-150-5p transfer via EVs in the context of I/R.
Main Methods:
- Establishment of rat models of I/R injury.
- Knockdown of TXNIP to assess its effects on myocardial remodeling.
- Culture of MSCs-derived EVs with cardiomyocytes under hypoxic/hypoglycemic conditions (in vitro).
- Intramyocardial injection of MSCs-derived EVs into I/R rats (in vivo).
- Assessment of myocardial infarction size (MIS), collagen volume fraction (CVF), and cardiomyocyte apoptosis.
Main Results:
- I/R-induced rats exhibited elevated TXNIP and reduced miR-150-5p levels, with increased cardiomyocyte apoptosis.
- MSCs-derived EVs successfully transferred miR-150-5p to cardiomyocytes.
- miR-150-5p delivery via EVs suppressed myocardial remodeling, indicated by smaller MIS and CVF, and reduced apoptosis.
- In vivo administration of miR-150-5p-loaded EVs in I/R rats downregulated TXNIP and attenuated myocardial remodeling.
Conclusions:
- MSCs-derived EVs facilitate miR-150-5p transfer, mitigating I/R-induced myocardial remodeling.
- The therapeutic effect involves the downregulation of TXNIP.
- This EV-mediated miRNA delivery represents a promising clinical strategy for treating I/R injury.
