Exosomal miR-150 partially attenuated acute lung injury by mediating microvascular endothelial cells and MAPK pathway

Background: Acute lung injury (ALI) is a respiratory disease with high morbidity and mortality rates. Currently, there is no effective treatment to complement mechanical ventilation. Exosomes and microRNAs (miRNAs) are promising agents for the management of this disease. Methods: Exosomes were isolated from mouse bone marrow stromal stem cells (BMSCs). The levels of two miRNAs, miR-542-3P and miR-150, in exosomes were determined using RT-PCR, and miR-150 was selected for further study. ALI model was established in mice using lipopolysaccharides, and then, they were treated with saline, exosomes, miRNA agomirs, or miRNA antagomirs. The concentrations of TNF-α, IL-6, and IL-1β and the number of neutrophils and macrophages in the bronchoalveolar lavage fluid were measured. The wet/dry weight ratio of the lung tissue was calculated, and tissue pathology and apoptosis were observed using hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. CD34 and VE-cadherin expression was detected using immunofluorescence. Proteins associated with apoptosis and MAPK signaling were detected using Western blotting, and miR-150 expression in lung tissue was evaluated using RT-PCR. Results: We successfully isolated BMSCs and exosomes and showed that the level of miR-150 was significantly higher than that of miR-542-3p. Exosomes and miR-150 reduced inflammation and lung edema while maintaining the integrity of the alveolar structure. They also mitigated microvascular endothelial cell injury by regulating the caspase-3, Bax/Bcl-2, and MAPK signaling. Conclusions: Exosomal miR-150 attenuates lipopolysaccharide-induced ALI through the MAPK pathway.