Abstract
A recently discovered key role of reactive oxygen species (ROS) in mitochondrial traffic has opened a wide alley for studying the interactions between cells, including stem cells. Since its discovery in 2006, intercellular mitochondria transport has been intensively studied in different cellular models as a basis for cell therapy, since the potential of replacing malfunctioning organelles appears to be very promising. In this study, we explored the transfer of mitochondria from multipotent mesenchymal stem cells (MMSC) to neural cells and analyzed its efficacy under normal conditions and upon induction of mitochondrial damage. We found that mitochondria were transferred from the MMSC to astrocytes in a more efficient manner when the astrocytes were exposed to ischemic damage associated with elevated ROS levels. Such transport of mitochondria restored the bioenergetics of the recipient cells and stimulated their proliferation. The introduction of MMSC with overexpressed Miro1 in animals that had undergone an experimental stroke led to significantly improved recovery of neurological functions. Our data suggest that mitochondrial impairment in differentiated cells can be compensated by receiving healthy mitochondria from MMSC. We demonstrate a key role of Miro1, which promotes the mitochondrial transfer from MMSC and suggest that the genetic modification of stem cells can improve the therapies for the injured brain.
Highlights
The role of reactive oxygen species (ROS) in vital cellular functions has become an axiom; their role in signal transduction is important for cell growth, differentiation, and death [1]
It is well known that ischemic stroke is associated with oxidative stress and severe impairments of mitochondrial functioning in the damaged brain region [35]
Numerous studies have demonstrated that the protection of the mitochondria of neural cells from damage can be an effective
Summary
The role of reactive oxygen species (ROS) in vital cellular functions has become an axiom; their role in signal transduction is important for cell growth, differentiation, and death [1]. Among these multi-faceted functions, special attention is deserved by recently discovered functions of ROS in mitochondrial traffic [2,3], which are directly related to the switch from normal to pathological cell functioning and vice versa. It has occurred that cell and mitochondrial technologies are inter-related, intercellular communication above all accounting for the interaction of stem cells with other cells. The last two types of cell interaction can lead to the exchange of cellular contents including organelles, such as mitochondria [8]
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