Background
Upon uptake by stressed cells, functional mitochondria can perform their normal functions, ultimately enhancing the survival of host cells. However, despite the promising
Conclusion
It is verified that F-Mito derived from BMSCs play a protective role in ischemia-reperfusion injury, as their weakening reduces microglial cell activation and alleviates neuroinflammation.
Methods
Functional mitochondria (F-Mito) were isolated from bone marrow-derived mesenchymal stem cells (BMSCs). The ability of microglia cells to internalize F-Mito was evaluated using a middle cerebral artery occlusion (MCAO) model in C57BL/6J mice and an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model. After OGD/R and F-Mito treatment, the temporal dynamics of intracellular reactive oxygen species (ROS) levels were examined.The relationship between ROS levels and F-Mito uptake was assessed at the individual cell level using MitoSOX, Mitotracker, and HIF-1α labeling.
Results
Our findings indicate that microglia cells exhibit enhanced mitochondrial uptake compared to astrocytes. Furthermore, internalized F-Mito reduced ROS levels and HIF-1α levels. Importantly, we found that the ROS response in microglia cells following ischemia is a critical regulator of F-Mito internalization, and promoting autophagy in microglia cells might reduce the uptake of ROS and HIF-1α levels.