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Table 2 MSC-EV RNA-mediated therapeutic effects

From: Molecular signatures of mesenchymal stem cell-derived extracellular vesicle-mediated tissue repair

Species/MSC origin

Injured organ/experimental model

Responsible RNA

Possible mechanisms for the therapeutic effect

Reference

Human/BM

Kidney/mouse model of AKI induced by glycerol (in vivo)

Predicted to be mRNAs

Induction of proliferation of surviving intrinsic epithelial cells

[29]

Human/BM

Kidney/mouse model of AKI induced by cisplatin (in vivo)

Predicted to be mRNAs

Induction of survival of tubular epithelial cells via anti-apoptotic effects

[30]

Human/BM

Kidney/rat model of AKI induced by ischemia/reperfusion (in vivo)

Predicted to be mRNAs

Proliferative and anti-apoptotic effects on surviving intrinsic epithelial cells

[31]

Human/BM

Lung/mouse endotoxin-induced or LPS-induced acute lung injury (in vivo)

KGF mRNA

Immunosuppressive effects partly through KGF elevation, which was caused by EV-mediated transfer of KGF mRNA

[32]

Rat/BM

Brain/rat model of middle cerebral artery occlusion (in vivo)

miR-133b

Induction of neurite outgrowth of neural cells

[33]

Rat/BM

Brain/rat model of middle cerebral artery occlusion (in vivo)

miR-133b

Promotion of functional recovery by increasing neuroblasts and induction of neurovascular plasticity by increasing vascular endothelial cells

[34]

Mouse/BM

Heart/mouse myocardial infarction model (in vivo)

miR-22

Reduction of apoptosis of ischemic cardiomyocytes by directly targeting methyl CpG binding protein 2 (Mecp2) via EV cargo miR-22

[35]

Rat/BM

Heart/rat regional MIR model (in vivo)

miRNA-19a

Reduction of the expression level of PTEN, a predicted target of miR-19a, thus activating the Akt and ERK signaling pathways

[37]

  1. AKI acute kidney injury, BM bone marrow, EV extracellular vesicle, KGF keratinocyte growth factor, LPS lipopolysaccharide, MIR myocardial ischemia/reperfusion, miRNA microRNA, MSC mesenchynal stem cell, PTEN phosphatase and tensin homolog