A research team in Delhi, India, has identified a protein that increases the transfer of mitochondria from mesenchymal stem cells to lung cells.
The delivery of mitochondria to human lung cells can rejuvenate damaged cells, they found.
The migration of mitochondria from stem cells to epithelial cells also helps to repair tissue damage and inflammation linked to asthma-like symptoms in mice.
The results show that the movement of mitochondria from stem cells to recipient cells is regulated by the protein Miro1 and is part of a well-directed process.
The introduction of mitochondria into damaged cells has beneficial effects on the health of cells and, in the long term, mesenchymal stem cells could even be engineered to create more effective therapies for lung disease in humans.
Earlier work revealed that mitochondria can be transferred between cells through tunneling nanotubes, thread-like structures formed from the plasma membranes of cells that bridge between different types of cells. Stem cells can also use tunneling nanotubes to transfer mitochondria to neighboring cells and the number of these nanotubes increases under conditions of stress.
In the study, the protein Miro1 was shown to regulate the transfer of mitochondria from mesenchymal stem cells to epithelial cells. Stem cells that were engineered to have higher amounts of Miro1 were able to transfer mitochondria more efficiently and were therapeutically more effective when tested in mouse models of airway injury and asthma, compared to untreated cells.
The researchers hope to determine how this pathway might translate into better stem cell therapies for human disease.