Table 3 MSC-EVs in the treatment of ALI/ARDS
From: Extracellular vesicles in the pathogenesis and treatment of acute lung injury
ALI | EVs source | Molecules | Target | Effect | References |
|---|---|---|---|---|---|
LPS | Endothelial progenitor cells-exosomes | miR-126 | Endothelial cells | Enhanced endothelial cell proliferation, migration, and tube formation; reduced permeability and inflammation | [6] |
LPS | Human iPSC-exosomes | Unknown | HMVECs | Inhibited ICAM-1 expression, and attenuated neutrophil adhesion | [83] |
Phosgene | MSC-EVs | Unknown | Lung tissues | Modulated inflammation, inhibited MMP-9 synthesis and elevated SP-C levels | [118] |
Traumatic | MSC-exosomes | miR-124-3P | Lung tissues | Inhibited P2X7 expression, suppressed inflammatory response and improved oxidative stress injury | [119] |
Burn | HUCMSC-exosomes | miR-451 | Lung tissues | Inhibited TLR4/NF-κB pathway/attenuated pulmonary inflammation | [120] |
Sulfur mustard | Bone marrow MSC-exosomes | Unknown | Epithelial cells | Inhibited epithelial cell apoptosis and restored epithelial barrier function | [122] |
Hyperoxia | Bone marrow MSC-exosomes | miR-425 | Lung tissues/RLE-6TN cells | Up-regulated PI3K/Akt signaling, increased cell viability, and reduced apoptosis | [123] |
Sepsis | MSC-exosomes | lncRNA-p21 | Lung tissues/ epithelial cells | Down-regulated miR-181 and up-regulated SIRT1 expression/suppressed epithelial cell apoptosis and prevented ALI | [124] |
LPS | MSC-EVs | Modified to exhibit miR-30b-3p | MLE-12 cells (mouse lung epithelial cells) | Increased cell proliferation and reduced apoptosis | [126] |
LPS | HUCMSC-EVs | miR-377-3p | Lung tissues | Suppressed the inflammatory factors and induced autophagy, ameliorated ALI | [127] |
Paraquat poisoning | DPSC-EVs | HGF | BESA-ZB | Inhibited the expression of pro-inflammatory factors and up-regulated the expression of anti-inflammatory factors | [128] |
Cigarette | MSC-EVs | Mitochondrial DNA | BEAS-2B cells | Regulated early mitochondrial genes involved in the fission/fusion process | [129] |
LPS | MSC-MVs | Ang-1 mRNA/HGF | Macrophages and HLMVECs | Maintained the integrity of microvascular endothelial cells and immunomodulatory properties of macrophages | |
Ventilator | ADSC-EVs | Unknown | Endothelial cells | Inhibited the TRPV4/Ca2+ pathway/suppressed pulmonary endothelial injury and inflammatory responses | [132] |
Histone | MSC-exosomes | miR-126 | HUVECs | Activated the PI3K/Akt pathway/attenuated endothelial cell apoptosis | [133] |
Ischemia–reperfusion | MSC-EVs | Unknown | Endothelial cells | Attenuated the activation of immune cells and restored the integrity of the endothelial cell barrier | [134] |
LPS | Endothelial progenitor cell-EVs | miR-126 | Endothelial cells | Down-regulated SPRED1 expression to activate RAF/ERK signaling, enhanced proliferation, migration and capillary tube formation | [135] |
LPS | MSC-exosomes | Unknown | Macrophages | Inhibited cellular glycolysis and M1 macrophage polarization | [136] |
LPS | MSC-EVs | Unknown | Alveolar macrophages | Improved autophagy/attenuated viability loss and apoptosis | [139] |
LPS | HUCMSC-exosomes | miRNA-22-3p | Alveolar macrophages | Inhibited inflammatory reaction and oxidative stress response, increased alveolar macrophage proliferation, and reduced macrophage apoptosis | [140] |
Escherichia coli endotoxin | MSC-MVs | KGF mRNA | Neutrophils | Reduced the influx of neutrophils and MIP-2 levels in BALF | [141] |
MDR-PA pneumonia | MSC-EVs | miR-466 | Neutrophils | Decreased influx of BALF neutrophils, proinflammatory factor levels and proteins | [142] |