Table 2.
MSC-EV RNA-mediated therapeutic effects
| 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] |
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