Downregulated miR-150 in bone marrow mesenchymal stem cells attenuates the apoptosis of LPS-stimulated RAW264.7 via MTCH2-dependent mitochondria transfer.

Mesenchymal stem cells (MSCs) are promising therapeutic cells for preventing apoptosis and abrogating cellular injury. Apoptosis of macrophages and the resulting dysfunction play a critical pathogenic role in acute respiratory distress syndrome (ARDS). Herein, the anti-apoptosis effects of bone marrow MSCs (BMSCs) on RAW264.7 were investigated by transwell assay. Compared to lipopolysaccharide (LPS) stimulation, the treatment of BMSCs decreased the level of cleaved caspase-3 protein, the ratio of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells, the level of caspase3-positive cells, and the accumulation of reactive oxygen species (ROS). Moreover, the expression of Bcl-2 and the level of mitochondrial membrane potential (MMP) were increased. Also, it was found that miR-150 disruption of BMSCs remarkably improved the efficiency of the treatment with LPS-stimulated RAW264.7 cells. The study demonstrated that the suppression of miR-150 facilitated the translation of MTCH2 gene and MTCH2-regulated mitochondria transfer from BMSCs to RAW264.7 cells, suggested that miR-150-mediated BMSCs has therapeutic potential for ARDS.