A team led by Professor Donald G. Phinney from the Florida campus of The Scripps Research Institute (TSRI) and Associate Professor Luis A. Ortiz from the University of Pittsburgh has shown for the first time how one set of specialized cells survives under stress by manipulating the behavior of key immune system cells.
The new research, presented lately in the journal Nature Communications, involved mesenchymal stem cells — which live in bone marrow and can differentiate between different cell kinds used in bone and connective tissue — and macrophages — which are immune cells that generally react to infectious agents or damaged cells by engulfing and devouring them.
Commenting on their research Phinney said,
“This is among the first few studies that has shown how mesenchymal stem cells cause their own survival by first increasing and then suppressing normal macrophage activity.” “This eventually puts the crosstalk between these cells into the perspective of cell survival.”
The team’s studies revealed that, like all other cells, mesenchymal stem cells encounter pressure due to tissue injury and inflammation. When this stress causes damage to the mitochondria, the mesenchymal stem cells hire the immune system’s macrophages — but in an uncommon way.
By re-engineering macrophage activity with secreted micro-RNA, the stem cells secure themselves from being attacked and instead package their impaired mitochondria into small sacs identified as vesicles and send them out to be surrounded by the macrophage.
Once macrophages subsume the broken mitochondria, the macrophages are capable of repackaging the mitochondria for their own use, restoring their own energy supplies. Preventing the exchange of impaired mitochondria to macrophages leads to death of the stem cells. Therefore, the procedure is mutually beneficial.
“It’s a transient phenomenon, which then enables the macrophages to use the mitochondria for their own surviving needs, all cells want to live; that’s what they do.”