Transplantation of astrocyte-derived mitochondria into injured astrocytes has a protective effect following stretch injury.

• Transplantation of astrocyte-derived mitochondria can improve cell viability, mitochondrial function and suppress apoptosis and inflammation in SI-damaged astrocytes. • Exogenous mitochondria isolated from untreated astrocytes can be incorporated into injured astrocytes and fuse with their mitochondrial networks. • The IKK/NF–κB and AMPK/PGC1α pathways in astrocytes may be involved in the anti-inflammatory effect and restoration of mitochondrial dysfunction mediated by mitochondrial transplantation. • The recovery of neuronal function caused by enhanced astrocytic support via astrocyte–neuron interactions might be a mechanism by which mitochondrial transplantation mitigates TBI-induced secondary injury. Traumatic brain injury (TBI) is a global public-health problem. Astrocytes, and their mitochondria, are important factors in the pathogenesis of TBI-induced secondary injury. Mitochondria extracted from healthy tissues and then transplanted have shown promise in models of a variety of diseases. However, the effect on recipient astrocytes is unclear. Here, we isolated primary astrocytes from newborn C57BL/6 mice, one portion of which was used to isolate mitochondria, and another was subjected to stretch injury (SI) followed by transplantation of the isolated mitochondria. After incubation for 12 h, cell viability, mitochondrial dysfunction, calcium overload, redox stress, inflammatory response, and apoptosis were improved. Live-cell imaging showed that the transplanted mitochondria were incorporated into injured astrocytes and fused with their mitochondrial networks, which was in accordance with the changes in the expression levels of markers of mitochondrial dynamics. The astrocytic IKK/NF–κB pathway was decelerated whereas the AMPK/PGC-1α pathway was accelerated by transplantation. Together, these results indicate that exogenous mitochondria from untreated astrocytes can be incorporated into injured astrocytes and fuse with their mitochondrial networks, improving cell viability by ameliorating mitochondrial dysfunction, redox stress, calcium overload, and inflammation. [ABSTRACT FROM AUTHOR]